Weinstock M, McCarty R
Proc Soc Exp Biol Med. 1983 Feb;172(2):194-201. doi: 10.3181/00379727-172-41545.
The cardiovascular effects of isoprenaline, methacholine, and sodium nitroprusside were studied in spontaneously hypertensive (SHR) and in Wistar-Kyoto normotensive (WKY) rats. In conscious rats with chronic indwelling arterial cannulae, methacholine caused a much greater fall in mean arterial blood pressure (MAP) in SHR rats, abolishing the initial 30-40 mm Hg difference in MAP at a dose of 2.5 micrograms/kg. The hypotensive response to methacholine was accompanied by reflex tachycardia in WKY rats but by a dose-related bradycardia in SHR rats. Isoprenaline increased heart rate and reduced blood pressure to a similar extent in rats of both strains. Administration of sodium nitroprusside resulted in a hypotensive response that was of greater duration in SHR rats. In addition, the reflex tachycardia was more marked and of greater duration in WKY compared to SHR rats. This demonstrates that the baroreflex response to vasodilation is suppressed in SHR rats and that this may contribute to the increased vasodepressor response of these animals to methacholine. However, when baroreflexes but not initial MAP were suppressed with pentobarbital, methacholine caused a similar degree of bradycardia in SHR and WKY rats but a greater vasodepressor response in SHR rats. With isoprenaline, the MAP difference between strains was maintained at all doses up to 200 ng/kg. Although it is not yet clear what is responsible for the increased vascular constriction of SHR rats, our findings suggest that it can be removed by muscarinic receptor activation with methacholine but not by stimulation of beta-adrenoceptors.
