The release of endogenous norepinephrine from the coccygeal artery of spontaneously hypertensive and Wistar-Kyoto rats.

The potassium (K+)-induced release of endogenous norepinephrine from the coccygeal artery of spontaneously hypertensive rats has been studied as a function of the development of hypertension. The absolute amount of norepinephrine released by potassium was greater in spontaneously hypertensive rat than the normotensive Wistar-Kyoto rat, regardless of age or blood pressure. However, the %-fractional release was elevated only in the rats with chronic hypertension. Preincubation of tissues with the alpha 2-antagonist, yohimbine, significantly enhanced norepinephrine overflow in all tissues studied. Young hypertensive animals demonstrated an enhancement equal to the Wistar-Kyoto rat controls. In the adult spontaneously hypertensive rat, however, there was a significantly lesser enhancement produced by yohimbine. Levels of norepinephrine in the nerves supplying the artery were greater in the prehypertensive spontaneously hypertensive rat than the age-matched Wistar-Kyoto rat. The norepinephrine content in arteries from adult animals was equivalent. The explanation for the attenuation of the yohimbine effect of chronic hypertensive animals is unclear. Although several explanations are possible, the data are consistent with the hypothesis that spontaneously hypertensive rats with chronic hypertension have subsensitive prejunctional alpha 2-receptors as evidenced by an increased %-fractional release of norepinephrine and a decreased enhancement of overflow in the presence of yohimbine. Clearly, further studies are needed to answer this provocative question and to understand the complex interactions of adrenergic neurotransmission in hypertensive animals.