Catecholaminergic regulation of venous function in the rainbow trout

Yutong Zhang, Leroy Weaver, Andrew Ibeawuchi, Kenneth Olson

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

The significance of the sympathetic nervous system (SNS) in regulating peripheral vascular resistance and cardiac function in fish has been well established, whereas its effect on venous function in vivo is unknown. Two protocols were employed in the present study to evaluate SNS effects on the venous system in intact, unanesthetized trout. In the first, trout were instrumented with pressure cannulas in the ventral (P(VA)) and dorsal (P(DA)) aortas and ductus Cuvier (P(VEN)), and cardiac output (CO) was measured with a flow probe around the ventral aorta. Heart rate, stroke volume, and gill and systemic resistances were calculated from the measured parameters. In the second group, vascular capacitance curves were obtained by monitoring mean circulatory filling pressure (P(VEN)) during transient interruption of CO and while blood volume was adjusted between 80 and 120% of normal. Unstressed blood volume (USBV) and vascular compliance (C) were derived from the capacitance curves. Infusion of epinephrine (Epi; 3.3 nmol · min-1 · kg body wt-1) increased P(VA), P(DA), and P(VEN), whereas norepinephrine (NE) infusion (3.3 nmol · min-1 · kg body wt-1) increased P(VA) and P(DA) but did not affect P(VEN). Epi (1.0 nmol · min-1 · kg body wt-1), but not NE (2.6 or 10.4 nmol · min-1 · kg body wt-1), displaced the capacitance curve to the right and significantly decreased USBV. Inhibition of α1-adrenoceptors with prazosin, or ganglionic nicotinic receptor blockade with hexamethonium, produced a left shift in the capacitance curve, and both treatments increased USBV and C. Conversely, the α-adrenoceptor antagonist phentolamine did not effect vascular capacitance. These results show that Epi has potent effects on trout veins in vivo and that it mobilizes blood from the unstressed into the stressed vascular compartment and augments central venous pressure by decreasing venous compliance. These results also show that the SNS is an active effector of venous tone and compliance in trout; this is the first demonstration of tonic regulation of vascular capacitance in any fish.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume274
Issue number4 43-4
StatePublished - Apr 1998

Fingerprint

Vascular Capacitance
Trout
Oncorhynchus mykiss
Blood Volume
Sympathetic Nervous System
Compliance
Cardiac Output
Vascular Resistance
Adrenergic Receptors
Blood Vessels
Aorta
Norepinephrine
Fishes
Pressure
Hexamethonium
Central Venous Pressure
Prazosin
Phentolamine
Nicotinic Receptors
Stroke Volume

Keywords

  • Cardiovascular control
  • Sympathetic nervous system
  • Unstressed volume
  • Vascular capacitance
  • Venous compliance

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Catecholaminergic regulation of venous function in the rainbow trout. / Zhang, Yutong; Weaver, Leroy; Ibeawuchi, Andrew; Olson, Kenneth.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 274, No. 4 43-4, 04.1998.

Research output: Contribution to journalArticle

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abstract = "The significance of the sympathetic nervous system (SNS) in regulating peripheral vascular resistance and cardiac function in fish has been well established, whereas its effect on venous function in vivo is unknown. Two protocols were employed in the present study to evaluate SNS effects on the venous system in intact, unanesthetized trout. In the first, trout were instrumented with pressure cannulas in the ventral (P(VA)) and dorsal (P(DA)) aortas and ductus Cuvier (P(VEN)), and cardiac output (CO) was measured with a flow probe around the ventral aorta. Heart rate, stroke volume, and gill and systemic resistances were calculated from the measured parameters. In the second group, vascular capacitance curves were obtained by monitoring mean circulatory filling pressure (P(VEN)) during transient interruption of CO and while blood volume was adjusted between 80 and 120{\%} of normal. Unstressed blood volume (USBV) and vascular compliance (C) were derived from the capacitance curves. Infusion of epinephrine (Epi; 3.3 nmol · min-1 · kg body wt-1) increased P(VA), P(DA), and P(VEN), whereas norepinephrine (NE) infusion (3.3 nmol · min-1 · kg body wt-1) increased P(VA) and P(DA) but did not affect P(VEN). Epi (1.0 nmol · min-1 · kg body wt-1), but not NE (2.6 or 10.4 nmol · min-1 · kg body wt-1), displaced the capacitance curve to the right and significantly decreased USBV. Inhibition of α1-adrenoceptors with prazosin, or ganglionic nicotinic receptor blockade with hexamethonium, produced a left shift in the capacitance curve, and both treatments increased USBV and C. Conversely, the α-adrenoceptor antagonist phentolamine did not effect vascular capacitance. These results show that Epi has potent effects on trout veins in vivo and that it mobilizes blood from the unstressed into the stressed vascular compartment and augments central venous pressure by decreasing venous compliance. These results also show that the SNS is an active effector of venous tone and compliance in trout; this is the first demonstration of tonic regulation of vascular capacitance in any fish.",
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AB - The significance of the sympathetic nervous system (SNS) in regulating peripheral vascular resistance and cardiac function in fish has been well established, whereas its effect on venous function in vivo is unknown. Two protocols were employed in the present study to evaluate SNS effects on the venous system in intact, unanesthetized trout. In the first, trout were instrumented with pressure cannulas in the ventral (P(VA)) and dorsal (P(DA)) aortas and ductus Cuvier (P(VEN)), and cardiac output (CO) was measured with a flow probe around the ventral aorta. Heart rate, stroke volume, and gill and systemic resistances were calculated from the measured parameters. In the second group, vascular capacitance curves were obtained by monitoring mean circulatory filling pressure (P(VEN)) during transient interruption of CO and while blood volume was adjusted between 80 and 120% of normal. Unstressed blood volume (USBV) and vascular compliance (C) were derived from the capacitance curves. Infusion of epinephrine (Epi; 3.3 nmol · min-1 · kg body wt-1) increased P(VA), P(DA), and P(VEN), whereas norepinephrine (NE) infusion (3.3 nmol · min-1 · kg body wt-1) increased P(VA) and P(DA) but did not affect P(VEN). Epi (1.0 nmol · min-1 · kg body wt-1), but not NE (2.6 or 10.4 nmol · min-1 · kg body wt-1), displaced the capacitance curve to the right and significantly decreased USBV. Inhibition of α1-adrenoceptors with prazosin, or ganglionic nicotinic receptor blockade with hexamethonium, produced a left shift in the capacitance curve, and both treatments increased USBV and C. Conversely, the α-adrenoceptor antagonist phentolamine did not effect vascular capacitance. These results show that Epi has potent effects on trout veins in vivo and that it mobilizes blood from the unstressed into the stressed vascular compartment and augments central venous pressure by decreasing venous compliance. These results also show that the SNS is an active effector of venous tone and compliance in trout; this is the first demonstration of tonic regulation of vascular capacitance in any fish.

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