The conduction of dilation along an arteriole is diminished in the cremaster muscle of hypertensive hamsters.

Arteriolar vasomotor responses can include a component that conducts along the vessel through gap junction channels. This study examined conducted vasomotor responses in arterioles of the hypertensive hamster. The cremaster muscle of normotensive (CHF-148) and spontaneously hypertensive (CHF-H4) hamsters was exteriorized. Micropipettes containing phenylephrine (0.1 M) or acetylcholine (ACh; 1.0 M) were positioned along second-order arterioles and diameter responses were recorded locally for every 0.4 mm upstream to 1.6 mm. Substantative local constrictions to phenylephrine(PE) were poorly conducted to the 0.4-mm site in normotensive and hypertensive hamsters. Local dilation to ACh decayed by 3 +/- 1 microm/mm as it conducted along arterioles of the normotensive hamster. In contrast, conducted dilation decayed by 7 +/- 1 microm/mm (p < 0.05) in the hypertensive hamster. This hypertension-induced increase in decay was reversed by alpha-adrenergic receptor blockade (phentolamine: 1 microM). However, arteriolar constriction to global alpha(1)- (PE) and alpha(2)- (clonidine) adrenergic agonists was unaffected by hypertension. Rather, sympathetic nervous activity was elevated in the hypertensive hamster as indicated by a greater reduction in arterial pressure upon sympathetic ablation (hexamethonium infusion: 30 mg/kg). This study provides the first evidence that vascular cell-cell communication is altered by the elevated sympathetic nervous activity observed in the hypertensive hamster.