Dependence of Vasoconstrictor Responses on Extracellular Calcium

Abstract

Vascular tone is regulated by metabolic, hormonal, ionic, and neuronal mechanisms. The adrenergic nervous system plays a major role in regulating vascular tone in physiologic and pathophysiologic states. Adrenergic stimulation increases vasoconstrictor tone by stimulating alpha adrenoceptors on the plasma membrane of resistance vessels. Recent studies have provided evidence that postsynaptic receptors with pharmacological properties similar to those of alpha-1 and alpha-2 adrenoceptors are present in the systemic and pulmonary vascular beds (1–6). It has been shown in in vivo studies that pressor responses to exogenous and neurogenically released norepinephrine may be mediated by different alpha adrenoceptor subtypes (2,7,8). In the canine hindlimb and pithed rat, responses to sympathetic nerve stimulation are selectively blocked by alpha-1 adrenoceptor antagonists whereas responses to exogenous norepinephrine are attenuated by alpha-2 adrenoceptor antagonists (2,7–9). It was, therefore, postulated that alpha-1 adrenoceptors are located intrasynaptically and are preferentially activated by neurogenically released norepinephrine whereas exogenous norepinephrine acts mainly on alpha-2 receptors which are located extrasynaptically (2,7,8). There are, however, exceptions to this concept in that neuronally released norepinephrine does not preferentially activate postjunctional alpha-1 adrenoceptors in isolated human blood vessels (10).