Vasodilator responses to K+ in genetic hypertensive and in renal hypertensive rats.

Vascular responses to K+ were studied in 37 genetically hypertensive (GH) rats of the New Zealand strain, 12 weight-matched and 11 age-matched normotensive control rats, 21 renal hypertensive (RH) rats with one renal artery clipped and the other kidney untouched, and 18 sham-clipped normotensive control (N) rats, under intravenous chloralose and pentobarbitol anesthesia. KCI in an isosmolar solution, delivering 1.84 X 10(-3), 3.07 X 10(-3), or 4.60 X 10(-3) mEq. K+ per minute was infused intra-arterially into the isolated pump-perfused (blood, 1 ml. per minute) hindlimb vascular beds, increasing measured limb arterial plasma [K+] up to 12 mEq. per liter without changing arterial pressure. The K+ infusions at all three rates reduced limb resistance (P less than 0.01). There was a linear correlation (P less than 0.01) between initial limb resistance and magnitude of response. Analysis of covariance indicated that there were no significant differences between responses in GH and normotensive control rats (P less than 0.1). In contrast, responses in RH rats were decreased (P less than 0.01) when compared to responses in N and GH rats. Thus, the vascular response to K+ is attenuated in renal hypertensive rats, as we have previously found in renal hypertensive dogs and essential hypertensive men, suggesting an underlying defect in vascular K+ metabolism. This abnormality is apparently not shared by genetically hypertensive rats of the New Zealand strain.