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Summary Twenty‐four hours after the last of 4 intravenous doses of 6‐hydroxydopamine (2×50 mg/kg on day 1 and 2×100 mg/kg on day 7) a complete impairment of adrenergic nerve function was observed in various organs of the rat. A complete recovery of adrenergic nerve function in vascular smooth muscle was observed 7 days after the last dose of 6‐hydroxydopamine whilst in non‐vascular smooth muscle recovery took between 14 and 21 days. On day 8, noradrenaline depletion produced by 6‐hydroxydopamine was not as great in vascular tissues, such as the mesentery and renal artery, as in other tissues, such as the heart and salivary glands. Noradrenaline concentrations recovered much more rapidly in vascular than in other tissues. Electron microscope studies of small mesenteric arteries showed a complete destruction of adrenergic nerve terminals 24 h after 6‐hydroxydopamine (2×100 mg/kg). However, there was a reappearance of growing terminals within 7 days and after 28 days the regrowth of adrenergic nerve terminals seemed complete. From the morphological and functional data it is concluded that 6‐hydroxydopamine does produce complete destruction of vascular adrenergic nerve terminals. However, these terminals regenerate more rapidly than those in other tissues. This could explain the failure of intravenously administered 6‐hydroxydopamine to prevent the development of experimental hypertension in the rat.

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Vascular resistance of the perfused whole body and isolated hindquarters was increased using preparations from renal, deoxycorticosterone/NaCl and genetic hypertensive rats. An increased reactivity to injected noradrenaline was observed in isolated perfused hindquarters from all three types of hypertensive rats. In depolarized mesenteric artery preparations, the calcium dose-response curves in preparations from normotensive and hypertensive rats were similar. The results point to structural changes of the blood vessels and a cellular hyperreactivity involving the process of excitation-contraction-coupling.