Unaltered maximum reflex vasodilatory capacity of the perfused hindquarters of spontaneously hypertensive rats.

Abstract

Hindquarter reflex vasodilation (RVD delta mmHg decrease in perfusion pressure) in response to arterial pressure elevations by intravenous norepinephrine (NE) was examined in young (2 1/2-3 months) and mature (8-10 months) spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) normotensive rats to ascertain whether maximum reflex vasodilatory capacity is altered in the developmental and/or established stages of spontaneous hypertension. The maximal RVD was not significantly different in young or mature SHR (young 26.2 +/- 1.9 and mature 36.2 +/- 3.2) compared to age-matched WKY controls (young 23.9 +/- 1.8 and mature 29.6 +/- 2.3) (P greater than 0.05 between SHR vs. WKY at both ages). However, the rise in mean systemic arterial pressure by NE which produced maximal RVD was greater in mature SHR (116.0 +/- 7.4 mmHg) than in WKY controls (78.3 +/- 6.2 mmHg) (P less than 0.01), whereas no such differences were found between young SHR (85.1 +/- 6.5 mmHg) and its WKY controls (87.5 +/- 2.3 mmHg). There was no difference in the dose of NE that required maximal responses of reflex vasodilation in young or mature SHR compared to WKY controls. In each age group of SHR or WKY rats, RVD was linearly related to the arterial pressure increments. The slope (a +/- SEM) of the regression line for the correlation between the pressure rises and resultant RVD was similar in young SHR (a = 0.424 +/- 0.061) and WKY controls of (a = 0.458 +/- 0.013). In contrast, the slope of the regression line for these two parameters in mature SHR (a = 0.250 +/- 0.004) was significantly smaller than that of either WKY controls (a = 0.364 +/- 0.010) or young SHR (P less than 0.01). The direct hindquarter vasodilation of mature SHR in response to intra-arterial administration of histamine or nitroglycerin was not different compared to that of WKY controls. The results indicate an unaltered maximum hindquarter reflex vasodilatory capacity during the developmental and established stages of genetic hypertension in SHR. An additional finding in the present study was the abnormal responsiveness of the baroreceptor reflex vasodilator system of mature SHR to a wide range of arterial pressure elevations. This abnormal responsiveness may contribute to the maintenance of high blood pressure in the established stage of hypertension.