Mechanism of elevation of hindquarter vascular resistance in spontaneously hypertensive rats.

In spontaneously hypertensive rats and normotensive control rats in the conscious state, hindquarter flow was observed with an electromagnetic flow probe chronically implanted around the terminal aorta. In separate groups of hypertensive and control rats, arterial pressure was observed with an indwelling catheter inserted into the terminal aorta. On ganglion blockade with hexamethonium bromide, hindquarter flow tended to increase in hypertensive rats and to decrease in normal rats. The percent change of hindquarter flow on ganglion blockade was significantly greater in the former than in the latter (p less than 0.05). Hindquarter peripheral resistance, estimated from flow and pressure values obtained in separate rat groups, was greater in hypertensive rats than in normal rats before ganglion blockade, but there was no difference between the groups after blockade. Presumably, an elevated sympathetic tone is responsible for the higher hindquarter peripheral resistance in spontaneously hypertensive rats, which plays an important part in the elevation of total peripheral resistance. However, bilateral lumbar sympathectomy did not induce chronic lowering of arterial pressure in hypertensive rats. This was at least partly due to the development of denervation supersensitivity.