Effect of verapamil and sodium nitroprusside on hindlimb vascular resistance in New Zealand genetically hypertensive and Japanese spontaneously hypertensive rats.

Verapamil, a calcium-entry blocker, and sodium nitroprusside, a non-specific vasodilator, were infused into the blood-perfused hindlimbs of New Zealand genetically hypertensive rats (NZGH) and spontaneously hypertensive rats (SHR), two genetic models of hypertension, and their normotensive controls, New Zealand normotensive rats and Wistar-Kyoto rats (WKY). Vasodilator responses, measured as the falls in perfusion pressure from the initial values, were similar and increased in NZGH and SHR. The responses were strongly dependent on the initial level of perfusion pressure in each strain of rat. It is concluded that increased vascular resistance, rather than a qualitative difference in vasodilator mechanisms, accounts for the enhanced responses to verapamil and sodium nitroprusside in NZGH and SHR hindlimbs.