title: Contributions of arginine vasopressin and the sympathetic nervous system to fulminating hypertension after destruction of neurons of caudal ventrolateral medulla in the rat.
abstract: We sought to determine the role in control of arterial pressure (AP) of the caudal ventrolateral medulla (CVL), a region containing noradrenergic neurons of the A1 group. Electrical stimulation of the A1 area in anaesthetized rats elicits a fall of AP and heart rate at low, but not high, stimulus frequencies. Electrolytic lesions of the A1 area produce fulminating hypertension and a 13-fold increase in plasma arginine vasopressin (AVP). A1-hypertension is attenuated by treatment with an AVP antagonist and is also diminished in rats of the Brattleboro strain. After AVP blockade, the residual hypertension is abolished by treatment with ganglionic or alpha adrenergic blockers, but not by adrenalectomy. We conclude that the region of the CVL containing the A1 noradrenergic cells tonically inhibits the discharge of sympathetic nerve activity as well as the release of AVP from the pituitary.
mesh_terms: D000311:Adrenal Glands / Q000502:physiology; D000315:Adrenalectomy; D000818:Animals; D001127:Arginine Vasopressin / Q000502:physiology*; D001794:Blood Pressure; D004558:Electric Stimulation; D006339:Heart Rate; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008526:Medulla Oblongata / Q000502:physiology*; D051381:Rats; D011910:Rats, Brattleboro; D011919:Rats, Inbred Strains; D013564:Sympathetic Nervous System / Q000502:physiology*
chemical_list: D001127:Arginine Vasopressin