Arteriolar proliferation in the rat cremaster muscle as a long-term autoregulatory response to reduced perfusion.

Long-term autoregulation of arterial blood flow to sustained increases or decreases in arterial pressure has been previously reported. It is not clear whether the adaptive process at the microscopic level is a modification of vessel caliber or density. The present study was undertaken to assess morphological and hemodynamic changes resulting from a sustained decrease in perfusion to the cremaster muscle in normal rats. The main feeding arteriole to the cremaster muscle was ligated at age 3 weeks in 11 male Wistar rats. At 6 weeks, the cremaster muscles on the ligated and control sides were evaluated microscopically for hemodynamic status and vascular architecture differences. Pressure was reduced 30% on the ligated side without a decrease in volume flow. This was possible because the number of second-order arterioles increased by 48% and the number of third-order arterioles increased by 98% on the ligated side. Although twice as many third-order arterioles were present in the ligated muscle, the same percentage was closed to flow in the resting state as in the control muscle (31 vs 29%). These findings are consistent with a long-term autoregulatory process which modulates arteriolar density in response to altered perfusion or distending pressure. The same process may be responsible for arteriolar rarefaction in response to sustained elevation in arterial pressure in the cremaster muscle of the spontaneously hypertensive rat (SHR).