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May 1, 1997EndocrinologyOpen Access

Atrial Natriuretic Peptide (ANP) Inhibits Its Own Secretion via ANPA Receptors: Altered Effect in Experimental Hypertension*

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Population

Conscious normotensive Sprague-Dawley rats, 1-yr-old conscious normotensive Wistar-Kyoto rats, and…

Comparison

i.v. infusion of ANP, CNP, or bolus… vs Basal conditions and acute volume expansion…

Design

Preclinical

Key result

Intravenous infusion of ANP blocked the plasma immunoreactive NT-ANP response to volume load (P < 0.001), showing that endogenous ANP directly modulates its own release via ANPA receptors.

Authors

HLHanna LeskinenOVOlli VuolteenahoMTMiklós Tóth

Discussion

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Overview

ANP autoregulation findings in animals warrant clinical caution; leaves open its role in human hypertension pending prospective data.

Structured PICO

P
Population
Conscious normotensive Sprague-Dawley rats, 1-yr-old conscious normotensive Wistar-Kyoto (WKY) rats, and spontaneously hypertensive rats (SHR)
I
Intervention
i.v. infusion of ANP (0.3 and 1.0 microg/kg x min), CNP, or bolus administration of HS-142-1 (1 or 3 mg/kg) under basal conditions and during acute volume expansion
C
Comparator
Basal conditions and acute volume expansion without the specific infusions
O
Outcome
Plasma levels of N-terminal fragment of pro-ANP (NT-ANP) and immunoreactive ANP (IR-ANP)surrogate

Main Result

p-value: p=<0.001

Endogenous ANP directly modulates its own release via ANPA receptors in vivo, and this modulation of acute volume expansion-induced atrial peptide release appears to be altered in experimental hypertension.

Cite This Study

Leskinen et al. (1997) studied Experimental hypertension. ANP, CNP, and HS-142-1 vs. Basal conditions and CNP was evaluated on Plasma levels of N-terminal fragment of pro-ANP (NT-ANP) and IR-ANP (p=<0.001). Intravenous infusion of ANP blocked the plasma immunoreactive NT-ANP response to volume load (P < 0.001), showing that endogenous ANP directly modulates its own release via ANPA receptors.

synapsesocial.com/papers/6a13d46e2398cfa26a890ef2https://doi.org/10.1210/endo.138.5.5120
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