Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The brain is one of the organs where an intrinsic renin-angiotensin system (RAS) has been described. Stimulation of circumventricular or brainstem angiotensin II (Ang II) receptors engenders a distinct pattern of cardiovascular, endocrine, and behavioral responses featuring blood pressure increase, attenuation of the baroreceptor reflex, drinking, release of pituitary hormones such as vasopressin, oxytocin, and ACTH, and natriuresis. In contrast to most of the other central actions of Ang II, the natriuretic effect cannot be elicited by Ang II as a circulating hormone. Recently, we have shown that stimulation of Ang II AT-1 receptors in the circumventricular organs causes a selective release of norepinephrine (NE) in the paraventricular nucleus (PVN) and in the supraoptic nucleus (SON). As vasopressin is also released from the PVN and SON, it is possible that the Ang II-NE interaction is involved in the release of vasopressin, thereby contributing to central blood pressure regulation and volume control. Finally, a substantial body of results suggests that an overactivity of the brain renin-angiotensin system is one of the contributors to genetic hypertension. However, this idea needs further confirmation.
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PMID:Role of brain angiotensin in cardiovascular regulation. 138 68

Hypothalamic and neurophypophyseal levels of catecholamines and peptides were measured in spontaneous and deoxycorticosterone (DOCA)/salt hypertension. Catecholamines, norepinephrine, epinephrine and dopamine were measured by electrochemical detection while the peptides, vasopressin, oxytocin, luteinizing hormone-releasing hormone (LHRH), the enkephalins and somatostatin (SRIF) were measured by radioimmunoassay. Blood pressure was significantly elevated in both groups as compared to their controls. Marked changes in central neural peptides were observed in the SHR, while no differences were seen in DOCA/salt hypertension. Hypothalamic vasopressin, oxytocin, LHRH and SRIF were significantly decreased. In the posterior pituitary, enkephalins were increased twofold in the SHR. With regard to catecholamines, there was no change in hypothalamic content. However, a dramatic decrease in neurohypophyseal dopamine was observed in SHR. Plasma levels of vasopressin were significantly elevated in both types of hypertension while oxytocin was increased only in the DOCA/salt model. These result show that (1) a wide spectrum of neuroendocrine changes are associated with genetic hypertension, (2) there are CNS differences between DOCA/salt and spontaneous hypertension, and (3) central aminergic changes may be involved in th neuroendocrine alterations seen in the SHR.
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PMID:Central neural peptides and catecholamines in spontaneous and DOCA/salt hypertension. 611 62

To investigate the role of arginine vasopressin (AVP) in genetic hypertension, we measured 24-h urinary volume, osmolality, and 24-h AVP excretion, as well as pituitary and pineal AVP and oxytocin levels, in genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) 5-and 45-week-old female rats of the Lyon strains. We also determined vascular sensitivity to AVP, norepinephrine, and angiotensin II in 6- and 21-week-old rats. AVP secretion was increased in both LH and LL rats compared with LN controls. Previous reports of increased AVP secretion in spontaneously hypertensive rats have suggested that AVP might play a role in high blood pressure. The existence of a similar increase in LL rats indicates that genetic hypertension of LH rats is not related directly to their increased AVP secretion. Furthermore, the vascular sensitivity to AVP was not specifically enhanced in 21-week-old LH rats compared with LN and LL controls. This study provides evidence against a major role of vasopressin in the genesis and maintenance of high blood pressure in this model of experimental hypertension, and emphasizes that the choice of controls in such investigations is of crucial importance.
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PMID:Vasopressin and oxytocin in genetically hypertensive rats of the Lyon strain. 619 19

The potential role of central neuroendocrine changes in the development of spontaneous hypertension was evaluated. The developmental changes in blood pressure and hypothalamic and plasma levels of vasopressin (AVP) and oxytocin (OT) were determined in groups of SHR and WKY animals from 3 to 24 weeks of age. Hypothalamic OT content was significantly lower in 3-, 6-, and 12-week-old SHR rats compared to age-matched WKY animals. Hypothalamic AVP content was not different at 3 weeks of age, but was lower in the SHRs at 6 and 12 weeks. To localize strain differences in AVP and OT, specific hypothalamic nuclei were removed from 300 microns frozen brain sections, and hormone content measured. Paraventricular AVP and OT content was lower in the SHRs which had increased blood pressure (6, 12, and 24 weeks of age) but not in the prehypertensive groups (3 weeks of age). Neuropeptide content was unchanged in the supraoptic nucleus or median eminence. Plasma levels of AVP were increased in the SHR, while OT was unchanged. Thus, genetic hypertension is associated with specific and localized changes in hypothalamic AVP and OT. The fact that the peptide deficit occurred in the paraventricular nucleus, a region thought to be involved in the control of autonomic function, may have important implications in terms of the pathogenesis of hypertension.
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PMID:Changes in paraventricular vasopressin and oxytocin during the development of spontaneous hypertension. 686 74

Oxytocin and its receptor are potentially important for cardiovascular functions. In the present paper, we report their chromosome locations in the rat and their comparative mapping with the mouse and human. They are located in chromosome regions previously known to contain quantitative trait loci for blood pressure in various genetic crosses. Thus, they have become valid candidate genes for genetic hypertension.
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PMID:Chromosomal and comparative mapping of rat oxytocin, oxytocin receptor and vasopressin genes. 1147 80

Abnormalities in dopamine production and receptor function have been described in human essential hypertension and rodent models of genetic hypertension. All of the five dopamine receptor genes (D1, D2, D3, D4, and D5) expressed in mammals and some of their regulators are in loci linked to hypertension in humans and in rodents. Under normal conditions, D1-like receptors (D1 and D5) inhibit sodium transport in the kidney and the intestine. However, in the Dahl salt-sensitive and spontaneously hypertensive rats, and humans with essential hypertension, the D1-like receptor-mediated inhibition of sodium transport is impaired because of an uncoupling of the D1-like receptor from its G protein/effector complex. The uncoupling is genetic, and receptor-, organ-, and nephron segment-specific. In human essential hypertension, the uncoupling of the D1 receptor from its G protein/effector complex is caused by an agonist-independent serine phosphorylation/desensitization by constitutively active variants of the G protein-coupled receptor kinase type 4. The D5 receptor is also important in blood pressure regulation. Disruption of the D5 or the D1 receptor gene in mice increases blood pressure. However, unlike the D1 receptor, the hypertension in D5 receptor null mice is caused by increased activity of the sympathetic nervous system, apparently due to activation of oxytocin, V1 vasopressin, and non-N-methyl D-aspartate receptors in the central nervous system. The cause of the activation of these receptors remains to be determined.
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PMID:D5 dopamine receptor knockout mice and hypertension. 1552 60