Modulation of jejunal ion and water absorption by endogenous angiotensin after hemorrhage.

In the pentobarbital sodium-anesthetized rat, hemorrhage of blood equivalent to 1% body weight (18.4% blood volume) increases plasma renin activity and plasma aldosterone concentration and also markedly elevates jejunal ion and water absorption. Infusion of angiotensin II (AII) also stimulates jejunal absorption, and in a manner similar to hemorrhage. The elevation of jejunal absorption in response to hemorrhage is not affected by removal of the adrenals but is totally inhibited by the converting enzyme inhibitor captopril and by bilateral nephrectomy. Thus, increased jejunal absorption following hemorrhage is mediated by the renin-angiotensin system and is not secondary to aldosterone release. Further experiments demonstrated that norepinephrine released from enteric sympathetic nerves controls jejunal absorption through activation of alpha-adrenergic receptors. The stimulation of jejunal absorption by tyramine was unaffected by propranolol but was totally abolished by phentolamine and by peripheral sympathectomy was 6-hydroxydopamine (intact adrenal medulla). The increase in jejunal absorption in response to hemorrhage also was unaffected by propranolol but was inhibited totally by phentolamine, prazosin, and peripheral sympathectomy. It is proposed that AII generated by hemorrhage facilitates norepinephrine release from enteric sympathetic nerves. The norepinephrine released by AII stimulates jejunal absorption by enhancing transepithelial transport processes or by altering the balance of Starling forces governing fluid absorption across enteric capillaries.