Pressure-flow curves reflect arteriolar responses in perfused rat hindquarters.

Results from studies using pump-perfused rat hindquarters are consistent with increased wall-to-lumen ratios in resistance vessels of spontaneously hypertensive rats (SHR). However, in vivo measurements of cremaster arterioles have not shown increased wall-to-lumen ratios in SHR. To investigate this discrepancy, we studied three groups of male SHR and Wistar-Kyoto rats at 12 weeks of age. In the first two groups, the cremaster muscle was prepared to allow microscopic observation while the hindquarters were pump-perfused with increasing concentrations of norepinephrine in oxygenated Tyrode's solution. Both groups of SHR showed an increase in vasodilated resistance and elevated maximal vasoconstrictor response. In the first group, arterioles showed dose-dependent constriction that was greater in smaller arterioles but did not differ between hypertensive and normotensive rats. Vasodilated diameters of second-order arterioles were significantly smaller in the hypertensive rats. In the second group, servo-null pressures in the first-order arteriole showed that the microvessels contributed proportionally to the elevation in resistance in both SHR and normotensive rats. In the third group, first- and second-order arterioles were measured in vivo and histologically. Arteriolar diameters did not differ between SHR and normotensive rats with either method. In fixed sections the cross-sectional area of the media-intima was greater in the SHR. Therefore, data from the pump-perfused rat hindquarters accurately reflect vasoconstrictor responses of the arterioles, and in deference to in vivo measurements on arteriolar walls that include the adventitia, the increased response in the SHR can be explained by hypertrophy of the arteriolar medial-intimal area.

Altered local regulation of blood flow and shear rate in renal hypertension.

The purpose of this study was to evaluate acute and chronic autoregulation of blood flow in the cremaster muscle of one-kidney, one-clip (1K1C) hypertensive rats and to investigate alterations of shear stress during the development of hypertension. Unilateral renal artery stenosis and contralateral nephrectomy were performed in half of the rats and a sham operation was carried out in the other half. Mean blood pressure was significantly increased at 1 (38%) and 4 (34%) weeks in 1K1C rats v age-matched controls. Heart rate was significantly increased 15% at 1 week in 1K1C rats but returned to the control level at 4 weeks. Cremaster arteriolar dimensions were measured in vivo by intravital microscopy. Resting diameter of the first-order arteriole (1A) in 1K1C rats was decreased by 25% (P < .05) at 1 week and by 16% at 4 weeks (ns). Measured by the dual-slit technique, total blood flow to the cremaster muscle in 1K1C rats was reduced by 58% (P < .05) at 1 week but was not significantly different from control at 4 weeks. Wall shear rate calculated in the 1A of 1K1C rats was not significantly different from control at 1 week but was elevated 70% (P < .05) at 4 weeks. Therefore, autoregulation of blood flow in skeletal muscle is impaired and/or overridden in the acute phase of 1K1C hypertension. Shear rate, however, did not deviate from the control level until later, which might be the result of impaired function of the endothelium in chronic hypertension.