KCl exacerbates hypertension (HT) in the strokeprone spontaneously hypertensive rats (SHRSP).

In the SHRSP, HT occurs without NaCl loading or apparent volume expansion, but is exacerbated by NaCl loading. Supplementing dietary potassium with KCl might also exacerbate HT because the Cl− component of either salt could further increase afferent arteriolar/renal vascular resistance which mediates both the exacerbation of HT, and the “paradoxical” increase in plasma renin activity (PRA) induced by NaCl loading. In the male SHRSP fed a low-normal NaCl diet (0.4%), we tested this hypothesis by comparing the effects of supplemented KCl, K citrate (Kcit), KHCO3 (KBC) and control CTL) on: 1) the progression of HT beginning 2 wks after surgically implanting a “Dataquest” pressor sensor in the abdominal aorta at 8 wks of age; 2) PRA at 25 wks. KCl exacerbated and KBC/Kcit attenuated HT within 6 wks of initiating their comparison; neither effect could be related to changes in body weight or urinary sodium excretion. PRA varied directly with BP. These observations suggest that in the SHRSP, Cl− and HCO−3 can differently modulate afferent arteriolar resistance and thereby the severity of HT and PRA.