Central and peripheral adrenergic modulation of carotid sinus-induced renin release

Harold D Schultz, J. E. Zehr, A. Livnat

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2 Citations (Scopus)

Abstract

To study central and peripheral mechanisms that regulate the level of circulating renin during activation of the carotid sinus baroreflex, both carotid sinuses were isolated and perfused at constant flow in chloralase-anesthetized dogs. Sinus pressure was controlled by an adjustable reservoir while systemic pressure was stabilized using an external chamber. Arterial renin activity, measured by radioimmunoassay, was increased during sinus hypotension only if systemic pressure was held constant. The renin response was eliminated by either sinus or renal denervation. Administration of propranolol (iv) or phentolamine directly into the renal artery totally blocked the increase in renin during activation of the reflex. Perfusion of a β-adrenergic blocker (propranolol) or an α-adrenergic blocker (phentolamine) though the third and fourth cerebroventricles had no effect on the increase in renin during sinus hypotension, whereas centrally administered clonidine, and α-agonist, blocked the response. We conclude that the sinus reflex arc affecting renin release involves not only activation of peripheral α- and β-adrenergic receptors in the kidney but also inhibition of central α-adrenergic receptors. No evidence for central β-involvement was found.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume11
Issue number2
StatePublished - Jan 1 1982

Fingerprint

Carotid Sinus
Renin
Adrenergic Agents
Adrenergic Antagonists
Phentolamine
Pressure
Propranolol
Hypotension
Adrenergic Receptors
Reflex
Kidney
Baroreflex
Clonidine
Denervation
Renal Artery
Radioimmunoassay
Perfusion
Dogs

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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N2 - To study central and peripheral mechanisms that regulate the level of circulating renin during activation of the carotid sinus baroreflex, both carotid sinuses were isolated and perfused at constant flow in chloralase-anesthetized dogs. Sinus pressure was controlled by an adjustable reservoir while systemic pressure was stabilized using an external chamber. Arterial renin activity, measured by radioimmunoassay, was increased during sinus hypotension only if systemic pressure was held constant. The renin response was eliminated by either sinus or renal denervation. Administration of propranolol (iv) or phentolamine directly into the renal artery totally blocked the increase in renin during activation of the reflex. Perfusion of a β-adrenergic blocker (propranolol) or an α-adrenergic blocker (phentolamine) though the third and fourth cerebroventricles had no effect on the increase in renin during sinus hypotension, whereas centrally administered clonidine, and α-agonist, blocked the response. We conclude that the sinus reflex arc affecting renin release involves not only activation of peripheral α- and β-adrenergic receptors in the kidney but also inhibition of central α-adrenergic receptors. No evidence for central β-involvement was found.

AB - To study central and peripheral mechanisms that regulate the level of circulating renin during activation of the carotid sinus baroreflex, both carotid sinuses were isolated and perfused at constant flow in chloralase-anesthetized dogs. Sinus pressure was controlled by an adjustable reservoir while systemic pressure was stabilized using an external chamber. Arterial renin activity, measured by radioimmunoassay, was increased during sinus hypotension only if systemic pressure was held constant. The renin response was eliminated by either sinus or renal denervation. Administration of propranolol (iv) or phentolamine directly into the renal artery totally blocked the increase in renin during activation of the reflex. Perfusion of a β-adrenergic blocker (propranolol) or an α-adrenergic blocker (phentolamine) though the third and fourth cerebroventricles had no effect on the increase in renin during sinus hypotension, whereas centrally administered clonidine, and α-agonist, blocked the response. We conclude that the sinus reflex arc affecting renin release involves not only activation of peripheral α- and β-adrenergic receptors in the kidney but also inhibition of central α-adrenergic receptors. No evidence for central β-involvement was found.

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