Adrenergic neurotransmission in vascular smooth muscle from spontaneously hypertensive rats.

Abstract

Adrenergic neurotransmission in isolated vascular smooth muscle from spontaneously hypertensive (SHR) and normotensive rats was compared. Tail arteries, excised from adult SHR and normotensive rats, were cut helically into strips that were mounted in organ chambers between 2 Pt wire electrodes. Isometric contractions were recorded. Vascular responsiveness was determined before and after acute denervation with 6-hydroxydopamine or before and after treatment with phentolamine. Release or displacement of endogenous norepinephrine was obtained with electrical stimulation, tyramine and K. The sensitivity to exogenous norepinephrine of innervated vessels was similar for SHR and normotensive rats. Denervation produced a significant shift to the left in the concentration-response curve to norepinephrine only in SHR vessels. Contractile responses to electrical stimulation, tyramine and K were similar in both groups before denervation. Contractile responses to K free solution were greater in SHR than in normotensive vessels. Following denervation, the SHR and normotensive vessels responded similarly to these latter interventions. Blockade of .alpha.-adrenoceptors with phentolamine reduced contractile responses to all agents in innervated and denervated vessels. Cocaine caused a slowing of the relaxation following contraction induced by electrical stimulation in both SHR and normotensive vessels. The relaxation of SHR vessels was less affected by cocaine than in normotensive vessels. The tissue content of norepinephrine was similar in SHR and normotensive arterial strips. In arterial strips from SHR the uptake of 3H-norepinephrine was significantly larger than in those from normotensive rats. The reactivity of innervated blood vessels to norepinephrine apparently is similar in SHR and normotensive rats. Important differences in sensitivity to norepinephrine in hypertensive vessels are unmasked when the relationship between the vascular smooth muscle cell and the adrenergic nerve terminal is altered. Apparently, the adrenergic nerve terminals in hypertensive blood vessels can modulate the junctional concentration of norepinephrine so that the contractile response to this agent is similar to that in normotensive blood vessels.