Reflex inhibition of plasma renin activity by increased left ventricular pressure in conscious dogs

• Published in: The American journal of physiology Vol. 256; no. 6 Pt 2; p. R1299
• Main Authors: Gorman, A J, Chen, J S
• Format: Journal Article
• Language: English
• Published: United States 01.06.1989
• Subjects: Animals; Aortic Valve Stenosis - physiopathology; Blood Pressure - drug effects; Dogs; Heart - physiology; Heart Conduction System - physiology; Heart Rate - drug effects; Heart Ventricles - physiopathology; Male; Nitroprusside - pharmacology; Reference Values; Reflex; Renin - blood; Renin-Angiotensin System; Ventricular Function
• ISSN: 0002-9513
• DOI: 10.1152/ajpregu.1989.256.6.R1299

The purpose of the present study was to determine the effects of left ventricular (LV) outflow obstruction on plasma renin activity (PRA) and the contribution from afferent receptors located in the LV myocardium. In chronically instrumented, conscious dogs (n = 12), changes in PRA during a 15- to 20-mmHg decrease in arterial blood pressure were assessed during 1) intravenous infusions of nitroprusside (NP) alone and 2) infusions of NP while peak systolic LV pressure was elevated by acute ascending aortic occlusion (AAO + NP). Infusions of NP alone elicited significant increases in heart rate (24.9 +/- 5.1 beats/min; P less than 0.01) and in PRA [3.31 +/- 0.53 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.01]. These were accompanied by decreases in both LV pressure (-13.8 +/- 3.6 mmHg; P less than 0.05) and left atrial pressure (-3.0 +/- 0.7 mmHg; P less than 0.05). During AAO + NP, LV pressure was elevated to an absolute level of 169.2 +/- 4.6 mmHg (+53.3 +/- 4.2 mmHg; P less than 0.001), whereas left atrial pressure was not changed. Both the hypotension-induced rise in PRA and tachycardia were significantly inhibited during AAO + NP (+0.59 +/- 0.29 ng ANG I.ml-1.h-1 and +6.3 +/- 4.6 beats/min, respectively; NS). The topical application of a local anesthetic in the region of the main coronary artery, sufficient to block the heart rate and arterial blood pressure responses to selective LV receptor stimulation by intracoronary veratridine (0.1-0.4 microgram/kg), resulted in significant increases in PRA and heart rate during AAO + NP.