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Kenneth R. Olson - One of the best experts on this subject based on the ideXlab platform.

  • Endogenous vascular synthesis of B-type and C-type natriuretic peptides in the rainbow trout.
    The Journal of experimental biology, 2011
    Co-Authors: Keven R Johnson, Todd M Hoagland, Kenneth R. Olson
    Abstract:

    In mammals, natriuretic peptides (NPs) lower blood pressure, reduce blood volume and broadly inhibit cardiovascular remodeling. NPs are often referred to as cardiac hormones, though they also have integral roles in regulating vascular tone, endothelial remodeling and inhibiting vascular smooth muscle cell hypertrophy. Two NPs [atrial (ANP) and C-type (CNP)] have been identified as endogenous constituents in the vasculature of mammals, though such a phenomenon has not previously been described in fishes. Here we describe the endogenous production of B-type NP (BNP) and CNP in multiple blood vessels of the rainbow trout. Western blot analysis showed pro-BNP and pro-CNP production in the efferent branchial artery, celiacomesenteric artery, ventral aorta and Anterior Cardinal Vein. The detection of pro-BNP and pro-CNP was also supported by MALDI-TOF mass spectrometry analysis of NP-enriched tissue extracts. Although vascular pro-peptide levels of BNP and CNP were quantitatively quite comparable to those found in reference tissues (the atrium for BNP and brain for CNP), mRNA levels of these NPs in the vasculature were greatly reduced as determined by quantitative PCR. When the evolutionarily conserved vascular NP (CNP) was infused into un-anesthetized trout, it reduced central venous pressure and mean circulatory filling pressure. CNP also decreased cardiac output via a reduction in preload. The presence of endogenous NP production in the trout vasculature and potent in vivo hypotensive effects further support the numerous functional similarities between teleost and mammalian NP systems.

  • C-type natriuretic peptide of rainbow trout (Oncorhynchus mykiss): primary structure and vasorelaxant activities.
    General and comparative endocrinology, 2003
    Co-Authors: Koji Inoue, Kenneth R. Olson, Michael J. Russell, Yoshio Takei
    Abstract:

    Natriuretic peptides (NPs) play important roles in osmoregulatory and cardiovascular systems of vertebrates. For functional studies of NPs, rainbow trout (Oncorhynchus mykiss), a euryhaline fish, is an interesting model. The information on homologous NPs of salmonid fish is, however, still incomplete with respect to C-type NP (CNP). In this study, we isolated cDNAs encoding the precursor of CNP from the brain of trout. Predicted mature CNP (CNP-22) sequence was identical to that of killifish Fundulus heteroclitus, and only one amino acid was different from that of the eel Anguilla japonica, demonstrating a greater conservation among different teleost species than is found with atrial NP (ANP) and ventricular NP (VNP). While the preprosegment of trout CNP retained 57% similarity to the eel sequence, similarities were low to those of sharks and tetrapods. The major site of expression identified by RT-PCR was the brain with minor expression in the atrium. The putative mature CNP-22 was synthesized and its biological activity was compared with other trout NPs (ANP and VNP) using trout ventral aorta, efferent branchial and celiacomesenteric arteries and Anterior Cardinal Vein in vitro. Synthetic trout CNP-22 relaxed all pre-contracted vessels with potencies comparable to trout ANP and VNP.

  • Effects of hypoxia on isolated vessels and perfused gills of rainbow trout
    Comparative biochemistry and physiology. Part A Molecular & integrative physiology, 2001
    Co-Authors: Michael P. Smith, Michael J. Russell, Jeffrey T. Wincko, Kenneth R. Olson
    Abstract:

    Abstract Local hypoxia dilates systemic and constricts pulmonary blood vessels in mammals without neural or humoral involvement. The direct effects of hypoxia on isolated vessels from bony fish have not been examined. In the present study, isolated vessels (efferent branchial artery, EBA; coeliacomesenteric artery, CMA; ventral aorta, VA; and Anterior Cardinal Vein, ACV) from rainbow or steelhead trout ( Oncorhynchus mykiss ) were subjected to either passive load (resting tension) or contracted with a ligand or 50 mM KCl and then subjected to 60 min of hypoxia by N 2 administration and an additional 30 min of normoxia. All vessels were usually refractory to hypoxia under conditions of resting tension. EBAs, CMAs and VAs pre-contracted with a receptor-mediated ligand were all significantly relaxed by hypoxia and only VAs recovered significantly upon subsequent restoration of normoxia. In contrast, tension in all arteries pre-contracted with 50 mM KCl was elevated further in response to hypoxia. Conversely, ligand-contracted ACVs responded to hypoxia with a further increase in tension, whereas KCl-contracted ACVs relaxed. During apparently random 2–3-week periods EBA and CMA from steelhead and EBA from rainbow trout were hyper-reactive to hypoxia. Steelhead vessels responded to hypoxia with a rapid contraction that increased in magnitude over 3 days. These contractions were independent of pre-stimulation and they were dose-dependent upon P o 2 . In isolated gills, hypoxic perfusate produced an immediate but transient elevation of resistance ( R GILL ) in all four gill arches. R GILL increased by as much as 30% of initial values and this response was unaltered upon a second hypoxic exposure. These studies demonstrate that isolated vascular segments of rainbow trout are indeed responsive to hypoxia and that these differential responses are vessel and tone dependent and the overall response may be altered by as yet unknown seasonal or environmental factors. Hypoxia-induced arterial relaxation is blocked by elevated external [K + ], implicating alteration of transmembrane K + conductance and/or membrane potential in this depressor response. K + -channel closure or voltage-gated Ca 2+ influx cannot account for arterial vasoconstriction due to hypoxia during KCl contractions. Vascular responses to hypoxia could have a profound impact on local flow in vivo and could mediate ventilation–perfusion matching in the branchial circulation of fish.

  • Pharmacological characterization of arginine vasotocin vascular smooth muscle receptors in the trout (Oncorhynchus mykiss) in vitro.
    General and Comparative Endocrinology, 1999
    Co-Authors: Daniel J. Conklin, Michael P. Smith, Kenneth R. Olson
    Abstract:

    Abstract Arginine vasotocin (AVT) is present in the neurohypophysis of all nonmammalian vertebrates and it appears to be the antecedent of the neurohypophysial nonapeptide hormones. Relatively little is known about AVT receptors in lower vertebrates, especially fish, and the present study was designed to examine AVT receptor interactions in trout vascular and nonvascular smooth muscle in vitro. AVT produced dose-dependent contraction of isolated rings from celiacomesenteric, coronary, and efferent branchial arteries, ventral aorta, Anterior Cardinal Vein, and strips of ductus Cuvier. The greatest efficacy (magnitude of contraction per unit tissue weight) and sensitivity (effective concentration for half-maximal response, EC 50 ) to AVT was found in the efferent bronchial artery (EBA) and its receptors were characterized further. Other neurohypophysial peptides, including arginine vasopressin (AVP), lysine vasopressin (LVP), isotocin (IST), and oxytocin (OXY), contracted EBA with an efficacy order of (most to least) AVT = AVP = OXY > LVP > IST and a sensitivity order of AVT > OXY ≥ AVP > IST > LVP. Neither Desmopressin, an AVP V 2 -receptor agonist, nor the AVP ring fragment, AVP 4–9 , contracted EBA nor did they inhibit AVT contraction. Pretreatment of EBA rings with the selective AVP V 1 -receptor antagonists (deamino-Pen 1 , O-Me-Tyr 2 , Arg 8 -vasopressin and deamino-Pen 1 , Val 4 , Arg 8 -vasopressin), the selective V 2 -receptor antagonist (adamantaneacetyl 1 , O-Et- d -Tyr 0 , Val 4 , aminobutyryl 6 , Arg 8,9 -vasopressin), or the combined V 1 -oxytocin receptor antagonist (d(CH 2 ) 5 [Tyr(Me) 2 , Orn 8 -AVT]) competitively inhibited AVT contractions without affecting AVT efficacy. Receptor affinity constants (pA 2 ) determined by Schild analysis were in the range of 6.8–7.3, with slightly higher constants for the AVP V 1 -/oxytocin receptor antagonists than for the selective V 2 -receptor antagonist. Endothelium removal had no effect on EBA sensitivity to AVT. EBA rings were an order of magnitude more sensitive to AVT than nonvascular gastrointestinal and urinary bladder smooth muscle rings or strips. However, AVT (10 −7 M) was as efficacious as acetylcholine (10 −5 M) in gastrointestinal, gallbladder, and urinary bladder smooth muscle. It is concluded that trout EBA possess an AVT smooth muscle receptor that shares a similar pharmacological profile with the mammalian vascular AVP V 1a -receptor and the OXY-receptor, but it is distinct from the previously reported gill epithelial cell receptor.

  • Cardiovascular effects of arginine vasotocin in the rainbow trout Oncorhynchus mykiss.
    The Journal of Experimental Biology, 1997
    Co-Authors: Daniel J. Conklin, Angelica Chavas, Douglas W. Duff, Leroy Weaver, Yutong Zhang, Kenneth R. Olson
    Abstract:

    The physiological functions of the neurohypophyseal hormone arginine vasotocin (AVT) in teleosts are not clear. In the present studies, the sites and mechanisms of action of AVT on the rainbow trout Oncorhynchus mykiss cardiovascular system were examined in unanesthetized instrumented fish, perfused organs and isolated vessels. Injection of AVT (1, 10 or 100 pmol kg-1 body mass) into trout with dorsal aortic cannulas produced a modest, but dose-dependent, increase in dorsal aortic pressure (PDA). Bolus injection of AVT (100 pmol kg-1 body mass), or continuous infusion (6.7 pmol kg-1 min-1), into trout instrumented with dorsal aortic, ventral aortic and central venous cannulas and a ventral aortic flow probe significantly increased PDA as well as ventral aortic (PVA) and central venous (PVEN) blood pressure. Bradycardia accompanied the rapid rise in PVA while gill resistance (RG) increased. Maximum response to the AVT bolus was reached within 13­21 min and the response decayed slowly over the ensuing 90 min. AVT infusion (6.7 pmol kg-1 min-1) significantly increased PVEN and mean circulatory filling pressure and decreased unstressed blood volume, whereas venous compliance was unaffected. These in vivo studies indicate that AVT increases venous tone, thereby mobilizing blood from the unstressed compartment into the stressed compartment. This increases PVEN, which increases venous return and helps maintain, or slightly elevate, cardiac output. This, combined with an elevated RG and slightly elevated systemic resistance (RS), increases both PVA and PDA; however, the rise in PDA is mitigated by a disproportionate increase in RG relative to RS. In vitro, the effects of AVT are consistent with in vivo responses. AVT increased vascular resistance in the perfused gill and perfused trunk and contracted isolated vascular rings from both rainbow and steelhead trout. The general order of sensitivity of isolated vessels to AVT was (in decreasing order): Anterior Cardinal Vein, celiacomesenteric artery, ductus Cuvier, efferent branchial artery, ventral aorta and coronary artery. Extracellular Ca2+ accounted for over 70 % of the tension in the AVT-contracted efferent branchial artery, but only 57 % of the tension in the Anterior Cardinal Vein. Vascular AVT receptor sensitivity (EC50) in vitro ranged from 0.3 to 6 nmol l-1 and was similar to the estimated ED50 for the dose-dependent increase in PDA in vivo (approximately 1 nmol l-1). AVT was not inotropic in paced ventricular rings nor did it exhibit vasorelaxant activity in perfused organs or vascular rings. These results show that AVT is a potent vasoconstrictor in trout and that its two primary cardiovascular targets are the systemic Veins and the branchial vasculature.

Daniel J. Conklin - One of the best experts on this subject based on the ideXlab platform.

  • Pharmacological characterization of arginine vasotocin vascular smooth muscle receptors in the trout (Oncorhynchus mykiss) in vitro.
    General and Comparative Endocrinology, 1999
    Co-Authors: Daniel J. Conklin, Michael P. Smith, Kenneth R. Olson
    Abstract:

    Abstract Arginine vasotocin (AVT) is present in the neurohypophysis of all nonmammalian vertebrates and it appears to be the antecedent of the neurohypophysial nonapeptide hormones. Relatively little is known about AVT receptors in lower vertebrates, especially fish, and the present study was designed to examine AVT receptor interactions in trout vascular and nonvascular smooth muscle in vitro. AVT produced dose-dependent contraction of isolated rings from celiacomesenteric, coronary, and efferent branchial arteries, ventral aorta, Anterior Cardinal Vein, and strips of ductus Cuvier. The greatest efficacy (magnitude of contraction per unit tissue weight) and sensitivity (effective concentration for half-maximal response, EC 50 ) to AVT was found in the efferent bronchial artery (EBA) and its receptors were characterized further. Other neurohypophysial peptides, including arginine vasopressin (AVP), lysine vasopressin (LVP), isotocin (IST), and oxytocin (OXY), contracted EBA with an efficacy order of (most to least) AVT = AVP = OXY > LVP > IST and a sensitivity order of AVT > OXY ≥ AVP > IST > LVP. Neither Desmopressin, an AVP V 2 -receptor agonist, nor the AVP ring fragment, AVP 4–9 , contracted EBA nor did they inhibit AVT contraction. Pretreatment of EBA rings with the selective AVP V 1 -receptor antagonists (deamino-Pen 1 , O-Me-Tyr 2 , Arg 8 -vasopressin and deamino-Pen 1 , Val 4 , Arg 8 -vasopressin), the selective V 2 -receptor antagonist (adamantaneacetyl 1 , O-Et- d -Tyr 0 , Val 4 , aminobutyryl 6 , Arg 8,9 -vasopressin), or the combined V 1 -oxytocin receptor antagonist (d(CH 2 ) 5 [Tyr(Me) 2 , Orn 8 -AVT]) competitively inhibited AVT contractions without affecting AVT efficacy. Receptor affinity constants (pA 2 ) determined by Schild analysis were in the range of 6.8–7.3, with slightly higher constants for the AVP V 1 -/oxytocin receptor antagonists than for the selective V 2 -receptor antagonist. Endothelium removal had no effect on EBA sensitivity to AVT. EBA rings were an order of magnitude more sensitive to AVT than nonvascular gastrointestinal and urinary bladder smooth muscle rings or strips. However, AVT (10 −7 M) was as efficacious as acetylcholine (10 −5 M) in gastrointestinal, gallbladder, and urinary bladder smooth muscle. It is concluded that trout EBA possess an AVT smooth muscle receptor that shares a similar pharmacological profile with the mammalian vascular AVP V 1a -receptor and the OXY-receptor, but it is distinct from the previously reported gill epithelial cell receptor.

  • Cardiovascular effects of arginine vasotocin in the rainbow trout Oncorhynchus mykiss.
    The Journal of Experimental Biology, 1997
    Co-Authors: Daniel J. Conklin, Angelica Chavas, Douglas W. Duff, Leroy Weaver, Yutong Zhang, Kenneth R. Olson
    Abstract:

    The physiological functions of the neurohypophyseal hormone arginine vasotocin (AVT) in teleosts are not clear. In the present studies, the sites and mechanisms of action of AVT on the rainbow trout Oncorhynchus mykiss cardiovascular system were examined in unanesthetized instrumented fish, perfused organs and isolated vessels. Injection of AVT (1, 10 or 100 pmol kg-1 body mass) into trout with dorsal aortic cannulas produced a modest, but dose-dependent, increase in dorsal aortic pressure (PDA). Bolus injection of AVT (100 pmol kg-1 body mass), or continuous infusion (6.7 pmol kg-1 min-1), into trout instrumented with dorsal aortic, ventral aortic and central venous cannulas and a ventral aortic flow probe significantly increased PDA as well as ventral aortic (PVA) and central venous (PVEN) blood pressure. Bradycardia accompanied the rapid rise in PVA while gill resistance (RG) increased. Maximum response to the AVT bolus was reached within 13­21 min and the response decayed slowly over the ensuing 90 min. AVT infusion (6.7 pmol kg-1 min-1) significantly increased PVEN and mean circulatory filling pressure and decreased unstressed blood volume, whereas venous compliance was unaffected. These in vivo studies indicate that AVT increases venous tone, thereby mobilizing blood from the unstressed compartment into the stressed compartment. This increases PVEN, which increases venous return and helps maintain, or slightly elevate, cardiac output. This, combined with an elevated RG and slightly elevated systemic resistance (RS), increases both PVA and PDA; however, the rise in PDA is mitigated by a disproportionate increase in RG relative to RS. In vitro, the effects of AVT are consistent with in vivo responses. AVT increased vascular resistance in the perfused gill and perfused trunk and contracted isolated vascular rings from both rainbow and steelhead trout. The general order of sensitivity of isolated vessels to AVT was (in decreasing order): Anterior Cardinal Vein, celiacomesenteric artery, ductus Cuvier, efferent branchial artery, ventral aorta and coronary artery. Extracellular Ca2+ accounted for over 70 % of the tension in the AVT-contracted efferent branchial artery, but only 57 % of the tension in the Anterior Cardinal Vein. Vascular AVT receptor sensitivity (EC50) in vitro ranged from 0.3 to 6 nmol l-1 and was similar to the estimated ED50 for the dose-dependent increase in PDA in vivo (approximately 1 nmol l-1). AVT was not inotropic in paced ventricular rings nor did it exhibit vasorelaxant activity in perfused organs or vascular rings. These results show that AVT is a potent vasoconstrictor in trout and that its two primary cardiovascular targets are the systemic Veins and the branchial vasculature.

  • Isolation and cardiovascular activity of a second bradykinin-related peptide ([Arg0,Trp5,Leu8]bradykinin) from trout
    Peptides, 1996
    Co-Authors: J. Michael Conlon, Daniel J. Conklin, Douglas W. Duff, Leroy Weaver, Jean-claude Le Mével, Kenneth R. Olson
    Abstract:

    Abstract Previous work has shown that incubation of heat-denatured plasma from the rainbow trout Oncorhynchus mykiss with porcine pancreatic kallikrein generates [Lys 0 ,Trp 5 ,Leu 8 ]bradykinin (trout [Lys 0 ]BK). We have now isolated a second BK-related peptide from kallikrein-treated trout plasma with the primary structure: Arg-Arg-Pro-Pro-Gly-Trp-Ser-Pro-Leu-Arg (trout [Arg 0 ]BK). Bolus injections of both trout [Arg 0 ]BK and [Lys 0 ]BK (>100 pmol/kg) into the dorsal aorta of conscious trout produced multiphasic effects on arterial blood pressure. An initial pressor response of short duration (1–2 min) was followed by a fall in pressure (to below basal values in 11 out of 15 animals) and then by a sustained rise in pressure lasting up to 60 min. The maximum rise in pressure produced by trout [Arg 0 ]BK (10 nmol/kg) was approximately one-fourth of the maximum rise produced by angiotensin II in the same animals. Intracerebroventricular injections of trout [Arg 0 ]BK (500 pmol) into conscious trout had no effect on arterial blood pressure or heart rate. Trout [Arg 0 ]BK did not affect the tension of vascular rings from trout efferent branchial and caeliacomesenteric arteries and Anterior Cardinal Vein. Trout des [Arg 9 ]BK had no effect on cardiovascular parameters, either in vivo or in vitro, indicating that the C -terminal arginine residue of the peptide is important in interaction with the trout kinin receptor(s).

Michael P. Smith - One of the best experts on this subject based on the ideXlab platform.

  • Effects of hypoxia on isolated vessels and perfused gills of rainbow trout
    Comparative biochemistry and physiology. Part A Molecular & integrative physiology, 2001
    Co-Authors: Michael P. Smith, Michael J. Russell, Jeffrey T. Wincko, Kenneth R. Olson
    Abstract:

    Abstract Local hypoxia dilates systemic and constricts pulmonary blood vessels in mammals without neural or humoral involvement. The direct effects of hypoxia on isolated vessels from bony fish have not been examined. In the present study, isolated vessels (efferent branchial artery, EBA; coeliacomesenteric artery, CMA; ventral aorta, VA; and Anterior Cardinal Vein, ACV) from rainbow or steelhead trout ( Oncorhynchus mykiss ) were subjected to either passive load (resting tension) or contracted with a ligand or 50 mM KCl and then subjected to 60 min of hypoxia by N 2 administration and an additional 30 min of normoxia. All vessels were usually refractory to hypoxia under conditions of resting tension. EBAs, CMAs and VAs pre-contracted with a receptor-mediated ligand were all significantly relaxed by hypoxia and only VAs recovered significantly upon subsequent restoration of normoxia. In contrast, tension in all arteries pre-contracted with 50 mM KCl was elevated further in response to hypoxia. Conversely, ligand-contracted ACVs responded to hypoxia with a further increase in tension, whereas KCl-contracted ACVs relaxed. During apparently random 2–3-week periods EBA and CMA from steelhead and EBA from rainbow trout were hyper-reactive to hypoxia. Steelhead vessels responded to hypoxia with a rapid contraction that increased in magnitude over 3 days. These contractions were independent of pre-stimulation and they were dose-dependent upon P o 2 . In isolated gills, hypoxic perfusate produced an immediate but transient elevation of resistance ( R GILL ) in all four gill arches. R GILL increased by as much as 30% of initial values and this response was unaltered upon a second hypoxic exposure. These studies demonstrate that isolated vascular segments of rainbow trout are indeed responsive to hypoxia and that these differential responses are vessel and tone dependent and the overall response may be altered by as yet unknown seasonal or environmental factors. Hypoxia-induced arterial relaxation is blocked by elevated external [K + ], implicating alteration of transmembrane K + conductance and/or membrane potential in this depressor response. K + -channel closure or voltage-gated Ca 2+ influx cannot account for arterial vasoconstriction due to hypoxia during KCl contractions. Vascular responses to hypoxia could have a profound impact on local flow in vivo and could mediate ventilation–perfusion matching in the branchial circulation of fish.

  • Pharmacological characterization of arginine vasotocin vascular smooth muscle receptors in the trout (Oncorhynchus mykiss) in vitro.
    General and Comparative Endocrinology, 1999
    Co-Authors: Daniel J. Conklin, Michael P. Smith, Kenneth R. Olson
    Abstract:

    Abstract Arginine vasotocin (AVT) is present in the neurohypophysis of all nonmammalian vertebrates and it appears to be the antecedent of the neurohypophysial nonapeptide hormones. Relatively little is known about AVT receptors in lower vertebrates, especially fish, and the present study was designed to examine AVT receptor interactions in trout vascular and nonvascular smooth muscle in vitro. AVT produced dose-dependent contraction of isolated rings from celiacomesenteric, coronary, and efferent branchial arteries, ventral aorta, Anterior Cardinal Vein, and strips of ductus Cuvier. The greatest efficacy (magnitude of contraction per unit tissue weight) and sensitivity (effective concentration for half-maximal response, EC 50 ) to AVT was found in the efferent bronchial artery (EBA) and its receptors were characterized further. Other neurohypophysial peptides, including arginine vasopressin (AVP), lysine vasopressin (LVP), isotocin (IST), and oxytocin (OXY), contracted EBA with an efficacy order of (most to least) AVT = AVP = OXY > LVP > IST and a sensitivity order of AVT > OXY ≥ AVP > IST > LVP. Neither Desmopressin, an AVP V 2 -receptor agonist, nor the AVP ring fragment, AVP 4–9 , contracted EBA nor did they inhibit AVT contraction. Pretreatment of EBA rings with the selective AVP V 1 -receptor antagonists (deamino-Pen 1 , O-Me-Tyr 2 , Arg 8 -vasopressin and deamino-Pen 1 , Val 4 , Arg 8 -vasopressin), the selective V 2 -receptor antagonist (adamantaneacetyl 1 , O-Et- d -Tyr 0 , Val 4 , aminobutyryl 6 , Arg 8,9 -vasopressin), or the combined V 1 -oxytocin receptor antagonist (d(CH 2 ) 5 [Tyr(Me) 2 , Orn 8 -AVT]) competitively inhibited AVT contractions without affecting AVT efficacy. Receptor affinity constants (pA 2 ) determined by Schild analysis were in the range of 6.8–7.3, with slightly higher constants for the AVP V 1 -/oxytocin receptor antagonists than for the selective V 2 -receptor antagonist. Endothelium removal had no effect on EBA sensitivity to AVT. EBA rings were an order of magnitude more sensitive to AVT than nonvascular gastrointestinal and urinary bladder smooth muscle rings or strips. However, AVT (10 −7 M) was as efficacious as acetylcholine (10 −5 M) in gastrointestinal, gallbladder, and urinary bladder smooth muscle. It is concluded that trout EBA possess an AVT smooth muscle receptor that shares a similar pharmacological profile with the mammalian vascular AVP V 1a -receptor and the OXY-receptor, but it is distinct from the previously reported gill epithelial cell receptor.

Yoshio Takei - One of the best experts on this subject based on the ideXlab platform.

  • C-type natriuretic peptide of rainbow trout (Oncorhynchus mykiss): primary structure and vasorelaxant activities.
    General and comparative endocrinology, 2003
    Co-Authors: Koji Inoue, Kenneth R. Olson, Michael J. Russell, Yoshio Takei
    Abstract:

    Natriuretic peptides (NPs) play important roles in osmoregulatory and cardiovascular systems of vertebrates. For functional studies of NPs, rainbow trout (Oncorhynchus mykiss), a euryhaline fish, is an interesting model. The information on homologous NPs of salmonid fish is, however, still incomplete with respect to C-type NP (CNP). In this study, we isolated cDNAs encoding the precursor of CNP from the brain of trout. Predicted mature CNP (CNP-22) sequence was identical to that of killifish Fundulus heteroclitus, and only one amino acid was different from that of the eel Anguilla japonica, demonstrating a greater conservation among different teleost species than is found with atrial NP (ANP) and ventricular NP (VNP). While the preprosegment of trout CNP retained 57% similarity to the eel sequence, similarities were low to those of sharks and tetrapods. The major site of expression identified by RT-PCR was the brain with minor expression in the atrium. The putative mature CNP-22 was synthesized and its biological activity was compared with other trout NPs (ANP and VNP) using trout ventral aorta, efferent branchial and celiacomesenteric arteries and Anterior Cardinal Vein in vitro. Synthetic trout CNP-22 relaxed all pre-contracted vessels with potencies comparable to trout ANP and VNP.

Michael J. Russell - One of the best experts on this subject based on the ideXlab platform.

  • C-type natriuretic peptide of rainbow trout (Oncorhynchus mykiss): primary structure and vasorelaxant activities.
    General and comparative endocrinology, 2003
    Co-Authors: Koji Inoue, Kenneth R. Olson, Michael J. Russell, Yoshio Takei
    Abstract:

    Natriuretic peptides (NPs) play important roles in osmoregulatory and cardiovascular systems of vertebrates. For functional studies of NPs, rainbow trout (Oncorhynchus mykiss), a euryhaline fish, is an interesting model. The information on homologous NPs of salmonid fish is, however, still incomplete with respect to C-type NP (CNP). In this study, we isolated cDNAs encoding the precursor of CNP from the brain of trout. Predicted mature CNP (CNP-22) sequence was identical to that of killifish Fundulus heteroclitus, and only one amino acid was different from that of the eel Anguilla japonica, demonstrating a greater conservation among different teleost species than is found with atrial NP (ANP) and ventricular NP (VNP). While the preprosegment of trout CNP retained 57% similarity to the eel sequence, similarities were low to those of sharks and tetrapods. The major site of expression identified by RT-PCR was the brain with minor expression in the atrium. The putative mature CNP-22 was synthesized and its biological activity was compared with other trout NPs (ANP and VNP) using trout ventral aorta, efferent branchial and celiacomesenteric arteries and Anterior Cardinal Vein in vitro. Synthetic trout CNP-22 relaxed all pre-contracted vessels with potencies comparable to trout ANP and VNP.

  • Effects of hypoxia on isolated vessels and perfused gills of rainbow trout
    Comparative biochemistry and physiology. Part A Molecular & integrative physiology, 2001
    Co-Authors: Michael P. Smith, Michael J. Russell, Jeffrey T. Wincko, Kenneth R. Olson
    Abstract:

    Abstract Local hypoxia dilates systemic and constricts pulmonary blood vessels in mammals without neural or humoral involvement. The direct effects of hypoxia on isolated vessels from bony fish have not been examined. In the present study, isolated vessels (efferent branchial artery, EBA; coeliacomesenteric artery, CMA; ventral aorta, VA; and Anterior Cardinal Vein, ACV) from rainbow or steelhead trout ( Oncorhynchus mykiss ) were subjected to either passive load (resting tension) or contracted with a ligand or 50 mM KCl and then subjected to 60 min of hypoxia by N 2 administration and an additional 30 min of normoxia. All vessels were usually refractory to hypoxia under conditions of resting tension. EBAs, CMAs and VAs pre-contracted with a receptor-mediated ligand were all significantly relaxed by hypoxia and only VAs recovered significantly upon subsequent restoration of normoxia. In contrast, tension in all arteries pre-contracted with 50 mM KCl was elevated further in response to hypoxia. Conversely, ligand-contracted ACVs responded to hypoxia with a further increase in tension, whereas KCl-contracted ACVs relaxed. During apparently random 2–3-week periods EBA and CMA from steelhead and EBA from rainbow trout were hyper-reactive to hypoxia. Steelhead vessels responded to hypoxia with a rapid contraction that increased in magnitude over 3 days. These contractions were independent of pre-stimulation and they were dose-dependent upon P o 2 . In isolated gills, hypoxic perfusate produced an immediate but transient elevation of resistance ( R GILL ) in all four gill arches. R GILL increased by as much as 30% of initial values and this response was unaltered upon a second hypoxic exposure. These studies demonstrate that isolated vascular segments of rainbow trout are indeed responsive to hypoxia and that these differential responses are vessel and tone dependent and the overall response may be altered by as yet unknown seasonal or environmental factors. Hypoxia-induced arterial relaxation is blocked by elevated external [K + ], implicating alteration of transmembrane K + conductance and/or membrane potential in this depressor response. K + -channel closure or voltage-gated Ca 2+ influx cannot account for arterial vasoconstriction due to hypoxia during KCl contractions. Vascular responses to hypoxia could have a profound impact on local flow in vivo and could mediate ventilation–perfusion matching in the branchial circulation of fish.