Humoral and mechanical factors modulating neural input to the renal vasculature

D. E. Carlson, Lawrence Schramm

Research output: Contribution to journalArticle

Abstract

The velocity and magnitude of neurally elicited renal vasoconstrictions decrease with reduction of renal arterial pressure. We investigated the relative roles of humoral and mechanical factors in this decrease. Cats were anesthetized with chloralose. Renal arterial pressure was controlled with an aortic cuff. Vasoconstrictions were elicited by electrical stimulation of the renal nerves until renal vascular resistance stabilized. Renal blood flow autoregulation was maintained during stimulation. Competitive blockade of angiotensin II did not affect the decrease in renal vascular responsiveness to neural input at reduced renal arterial pressure. A mathematical model suggested that a major portion of the decrease in the velocity of vasoconstrictions was a mechanical consequence of autoregulatory vasodilation. However, the model the blockade of prostaglandin synthesis, and this blockade significantly increase the velocity of vasoconstrictions at renal arterial pressures of 75 Torr or below. These results suggested that prostaglandins as well as mechanical factors played a role in the autoregulatory decrease in responsiveness to sympathetic input.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume4
Issue number1
StatePublished - 1978

Fingerprint

Kidney
Vasoconstriction
Arterial Pressure
Prostaglandins
Chloralose
Renal Circulation
Vasodilation
Angiotensin II
Vascular Resistance
Electric Stimulation
Blood Vessels
Cats
Homeostasis
Theoretical Models

ASJC Scopus subject areas

  • Physiology

Cite this

@article{75b04e8de4d842d78034a77704281ded,
title = "Humoral and mechanical factors modulating neural input to the renal vasculature",
abstract = "The velocity and magnitude of neurally elicited renal vasoconstrictions decrease with reduction of renal arterial pressure. We investigated the relative roles of humoral and mechanical factors in this decrease. Cats were anesthetized with chloralose. Renal arterial pressure was controlled with an aortic cuff. Vasoconstrictions were elicited by electrical stimulation of the renal nerves until renal vascular resistance stabilized. Renal blood flow autoregulation was maintained during stimulation. Competitive blockade of angiotensin II did not affect the decrease in renal vascular responsiveness to neural input at reduced renal arterial pressure. A mathematical model suggested that a major portion of the decrease in the velocity of vasoconstrictions was a mechanical consequence of autoregulatory vasodilation. However, the model the blockade of prostaglandin synthesis, and this blockade significantly increase the velocity of vasoconstrictions at renal arterial pressures of 75 Torr or below. These results suggested that prostaglandins as well as mechanical factors played a role in the autoregulatory decrease in responsiveness to sympathetic input.",
author = "Carlson, {D. E.} and Lawrence Schramm",
year = "1978",
language = "English (US)",
volume = "4",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "1",

}

TY - JOUR

T1 - Humoral and mechanical factors modulating neural input to the renal vasculature

AU - Carlson, D. E.

AU - Schramm, Lawrence

PY - 1978

Y1 - 1978

N2 - The velocity and magnitude of neurally elicited renal vasoconstrictions decrease with reduction of renal arterial pressure. We investigated the relative roles of humoral and mechanical factors in this decrease. Cats were anesthetized with chloralose. Renal arterial pressure was controlled with an aortic cuff. Vasoconstrictions were elicited by electrical stimulation of the renal nerves until renal vascular resistance stabilized. Renal blood flow autoregulation was maintained during stimulation. Competitive blockade of angiotensin II did not affect the decrease in renal vascular responsiveness to neural input at reduced renal arterial pressure. A mathematical model suggested that a major portion of the decrease in the velocity of vasoconstrictions was a mechanical consequence of autoregulatory vasodilation. However, the model the blockade of prostaglandin synthesis, and this blockade significantly increase the velocity of vasoconstrictions at renal arterial pressures of 75 Torr or below. These results suggested that prostaglandins as well as mechanical factors played a role in the autoregulatory decrease in responsiveness to sympathetic input.

AB - The velocity and magnitude of neurally elicited renal vasoconstrictions decrease with reduction of renal arterial pressure. We investigated the relative roles of humoral and mechanical factors in this decrease. Cats were anesthetized with chloralose. Renal arterial pressure was controlled with an aortic cuff. Vasoconstrictions were elicited by electrical stimulation of the renal nerves until renal vascular resistance stabilized. Renal blood flow autoregulation was maintained during stimulation. Competitive blockade of angiotensin II did not affect the decrease in renal vascular responsiveness to neural input at reduced renal arterial pressure. A mathematical model suggested that a major portion of the decrease in the velocity of vasoconstrictions was a mechanical consequence of autoregulatory vasodilation. However, the model the blockade of prostaglandin synthesis, and this blockade significantly increase the velocity of vasoconstrictions at renal arterial pressures of 75 Torr or below. These results suggested that prostaglandins as well as mechanical factors played a role in the autoregulatory decrease in responsiveness to sympathetic input.

UR - http://www.scopus.com/inward/record.url?scp=0018242939&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018242939&partnerID=8YFLogxK

M3 - Article

VL - 4

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 1

ER -