What does this research mean for the field?

Renal sympathetic nerves mediate intrarenal vasoconstriction during congestive heart failure and volume depletion through both direct constrictor actions on glomerular vessels and the stimulation of angiotensin II release. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

November 1, 1985Journal of Clinical InvestigationOpen Access

Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion.

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Why the study?

Does acute renal denervation improve renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion?

Population

Adult male Munich-Wistar rats weighing 183-369 g, including models of congestive heart failure secondary to…

Comparison

Acute renal denervation and/or intravenous… vs Baseline measurements before denervation…

Design

Preclinical

Follow-up

Acute (measurements taken 45-120 minutes post-denervation)

Authors

VKValentina KonCross-Cutting Cardiology AYAida YaredBoston University IIIekuni IchikawaShinshu University

Discussion

Member takes

Implication

Should not yet change practice; extends preclinical evidence on renal hemodynamics in experimental heart failure.

Structured PICO

Does acute renal denervation improve renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion?

Population

Adult male Munich-Wistar rats weighing 183-369 g, including models of congestive heart failure secondary to surgically induced myocardial infarction (n=10), acute extracellular fluid volume depletion via 48 h water deprivation (n=53), and sham-operated or nontreated controls (n=6).

Intervention

Acute renal denervation (surgical severing of nerve bundles and 10% phenol swabbing) and/or intravenous saralasin (angiotensin II antagonist, 0.3 mg/kg/h).

Comparator

Baseline measurements before denervation (within-subject comparison), sham-operated/nontreated controls, or saralasin alone.

Outcome

Renal cortical microcirculation parameters including glomerular plasma flow rate (QA), single nephron glomerular filtration rate (SNGFR), and afferent/efferent arteriolar resistances.surrogate

Renal sympathetic nerves play a pathophysiologic role in mediating renal vasoconstriction and hypoperfusion during experimental heart failure and volume depletion, acting partly via angiotensin II stimulation.

Limitations

Theoretical possibility that angiotensin II may only be partially inhibited by saralasin

Cite This Study

Kon et al. (1985) studied this question.

synapsesocial.com/papers/6a154bdc37103a43379f84ea https://doi.org/10.1172/jci112187

Topics

Heart failure HFrEF treatment

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Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion.

Discussion

Member takes

Implication

Structured PICO

Limitations

Cite This Study

Topics

Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion.

Discussion

Member takes

Implication

Structured PICO

Limitations

Cite This Study

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Topics

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