Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin II receptor and angiotensin converting enzyme distributions in the human medulla oblongata were localised by quantitative in vitro autoradiography. Angiotensin II receptors were labelled with the antagonist analogue 125I-[Sar1, Ile8] AII while angiotensin converting enzyme was labelled with 125I-351A, a derivative of the specific converting enzyme inhibitor, lisinopril. Angiotensin II receptor binding and angiotensin converting enzyme are present in high concentrations in the nucleus of the solitary tract, the dorsal motor nucleus of vagus, the rostral and caudal ventrolateral reticular nucleus, and in a band connecting the dorsal and ventral regions. In the rostral and caudal ventrolateral reticular nucleus, angiotensin II receptors are distributed in a punctate pattern that registers with neuronal cell bodies. The distribution and density of these cell bodies closely resemble those of catecholamine-containing neurones mapped by others. In view of the known interactions of angiotensin II with both central and peripheral catecholamine-containing neurons of laboratory animals, the current anatomical findings suggest similar interactions between these neuroactive compounds in the human central nervous system. The presence of angiotensin II receptors and angiotensin converting enzyme in the nucleus of the solitary tract, dorsal motor nucleus of vagus, and rostral and caudal ventrolateral reticular nucleus demonstrates sites for central angiotensin II to exert its known actions on vasopressin release and autonomic functions including blood pressure control. These data also suggest a possible interaction between angiotensin II and central catecholeminergic systems.
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PMID:Localization and characterization of angiotensin II receptor binding and angiotensin converting enzyme in the human medulla oblongata. 283 36

Angiotensin II receptor antagonists (AT-1) represent a new group of orally active antihypertensive agents. Activation on AT-1 receptor leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone with production of thirst, and promote growth of vascular and cardiac muscle; these effects are blocked by AT-1 antagonist agents. The first chemically useful, orally active AT-1 receptor antagonist was losartan, followed by other agents currently in clinical use, such as: valsartan, eprosartan, irbesartan, telmisartan, candesartan, and many others under investigation. AT-1 receptor antagonists are effective in reducing high blood pressure in hypertensive patients. Monotherapy in mild to moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of a thiazide diuretic is added, 60 to 70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme inhibitors, diuretics, calcium antagonists and beta-blocking agents. Tolerability has been reported to be very good. AT-1 receptor antagonists would be a drug of choice in otherwise well-controlled hypertensive patients treated with angiotensin-converting enzyme inhibitors who developed cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted.
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PMID:Angiotensin II receptor antagonists in arterial hypertension. 1085 84

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.
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PMID:Angiotensin II receptor antagonists role in arterial hypertension. 1198 4

Abstract Stimulation of the caudal ventrolateral medulla in rats and rabbits elicits secretion of vasopressin from the neurohypophysis. Inhibition of the area attenuates baroreceptor-initiated vasopressin secretion. Angiotensin II receptor binding sites and angiotensin-like immunoreactive nerve terminals are localized in the caudal ventrolateral medulla, in the region of the A1 noradrenaline-synthesizing neurons. To examine the possible functional role of angiotensin II in this region, we have microinjected angiotensin II into the A1 area in the urethane-anaesthetized rabbit. Microinjection of angiotensin II (0.1 to 100 pmol in 100 nl) stimulated vasopressin secretion (plasma vasopressin concentration increased from 24 +/- 8 pg/ml to 104 +/- 8 pg/ml following microinjection of 10 pmol angiotensin II) and produced a depressor response with bradycardia. The responsive area was confined to the region of the A1 cell group. AII responses were blocked by prior intramedullary injection of an angiotensin II receptor antagonist, [Sar(1), Thr(8)] angiotensin II (2 nmol in 200 nl), which had no effect on the response to the excitatory amino-acid N-methyl-D-aspartate. Following spinal blockade of efferent sympathetic activity, microinjections of angiotensin II into the caudal ventrolateral medulla caused a similar increase in plasma vasopressin concentration without a depressor response, demonstrating that the stimulation of vasopressin release by angiotensin II was not secondary to hypotension. Microinjection of [Sar(1), Thr(8)] angiotensin II dramatically attenuated the normal secretion of vasopressin in response to systemic haemorrhage. Following injection of vehicle into the caudal ventrolateral medulla, haemorrhage stimulated an increase in plasma vasopressin concentration from 3 +/- 1 pg/ml to 335 +/- 75 pg/ ml (n = 5). After microinjection of [Sar(1), Thr(8)] angiotensin II the haemorrhage-induced change in vasopressin concentration was only 17 +/- 6 pg/ml to 35 +/- 7 pg/ml (n = 4). Microinjection of the N-methyl-D-aspartate receptor antagonist, DL-amino-5-phosphonovaleric acid (5 nmol, n = 4), did not alter the secretion of vasopressin in response to haemorrhage. These results in the anaesthetized rabbit suggest that angiotensin II in the caudal ventrolateral medulla may have a physiological role in baroreceptor control of vasopressin release.
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PMID:Vasopressin Release Following Microinjection of Angiotensin II into the Caudal Ventrolateral Medulla Oblongata in the Anaesthetized Rabbit. 1921 31