Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropeptide Y (NPY), first isolated in 1982, is widely distributed among the neurons of the central and peripheral nervous systems, often in close association with catecholamines. Because of its wide distribution and concentrations in selected areas of the brain, NPY is considered a putative neurotransmitter with several possible physiological effects including modulation of blood pressure, food intake and pituitary hormone release at a central level. Peripherally, the peptide seems to be involved, via direct and indirect mechanisms, in noradrenaline (NA)-mediated vasoconstriction. The ability of NPY to interact with the catecholamine transmission line may underly a possible modulatory influence of NPY on catecholamine receptor characteristics. We recently observed interaction between alpha-2 adrenergic receptors and those for NPY at the presynaptic level. Additional data from our studies in spontaneously hypertensive rats suggest that impairment of these interactions may contribute to the hypertension in this strain.
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PMID:Neuropeptide Y interaction with the adrenergic transmission line: a study of its effect on alpha-2 adrenergic receptors. 132 37

Neuropeptide Y (NPY) has a wide and specific distribution in the central nervous system, and is colocalized with catecholamines in specific neuronal systems. In this study, in order to investigate the regulatory mechanisms of NPY and presynaptic alpha 2-adrenergic receptors on central noradrenergic transmission in hypertension, we have examined the effects of NPY and the alpha 2-agonist, UK 14,304, on (3H)-noradrenaline (NA) release from hypothalamic slices of spontaneously hypertensive rats (SHR). Electrical stimulation (1 Hz)-evoked (3H)-NA release was significantly greater in the hypothalamic slices of SHR than in those of Wistar Kyoto rats (WKY). NPY and the alpha 2-agonist, UK 14,304, inhibited the stimulation-evoked (3H)-NA release in a dose-related manner. The inhibitory effects of NPY and UK 14,304 on NA release were significantly attenuated in SHR compared with WKY. These results suggest that NPY and alpha 2-adrenoceptors might be involved in the regulation of central sympathetic nervous activity in hypertension.
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PMID:Modulation of noradrenergic transmission by neuropeptide Y and presynaptic alpha 2-adrenergic receptors in the hypothalamus of spontaneously hypertensive rats. 135 Jun 45

The mechanisms of hypertension during primary hyperaldosteronism and Cushing's syndrome are not completely understood. An enhanced vascular sensitivity to noradrenaline has been described in both situations. Neuropeptide Y (NPY) induces direct vasoconstriction and potentiates the action of noradrenaline. Sodium retention and dexamethasone have been shown to increase circulating NPY levels in animals and the expression of NPY in neuroendocrine cells. In order to determine if NPY could be involved in the enhanced vascular sensitivity to noradrenaline associated with adrenocortical hyperactivity, we measured plasma NPY in patients with Cushing's syndrome (n = 26) and primary hyperaldosteronism (n = 15) and compared it with that of hypertensive patients with pheochromocytomas (n = 13) or essential hypertension (n = 51) and with normotensive controls (n = 47). The concentration of NPY-Like immunoreactivity (NPY-Li) (mean +/- S.E.) in controls was 39.6 +/- 3.0 pg/ml. Elevated concentrations were found in 77% of the samples collected from pheochromocytoma patients (1180.4 +/- 394.0 pg/ml). NPY-Li levels in patients with essential hypertension (35.0 +/- 2.6 pg/ml), primary hyperaldosteronism (31.3 +/- 3.9 pg/ml) and Cushing's syndrome (33.1 +/- 4.8 pg/ml) were not different from that of controls. NPY-Li levels in hypertensive and normotensive patients with Cushing's syndrome were similar (38.5 +/- 7.5 vs 24.2 +/- 3.7 pg/ml). No correlation was found between the NPY-Li level and the mean blood pressure at the time of sampling. Our results suggest that NPY is unlikely to be involved in the pathogenesis of hypertension associated with primary hyperaldosteronism and Cushing's syndrome.
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PMID:Plasma concentration of neuropeptide Y in patients with adrenal hypertension. 147 6

Neuropeptide Y (NPY) is coreleased with noradrenaline (NA) from sympathetic nerve endings. In vitro data suggest that NPY is coreleased during high stimulation frequencies. The present study investigates plasma levels of catecholamines and neuropeptide Y (NPY) during changes in sympathetic nervous activity in conscious dogs. Increase in sympathetic tone: arterial hypertension elicited by sinoaortic denervation induced an increase (X 2) in plasma noradrenaline (NA) but no change in NPY levels. High (0.5 mg/kg i.v.) but not low (0.05 mg/kg i.v.) doses of yohimbine rose plasma NPY concentrations. Decrease in sympathetic tone: clonidine (10 micrograms/kg i.v.) but not beta-blocking agents (propranolol or atenolol: 1 mg/kg i.v.) reduced plasma NPY levels. These results show that NPY is correleased in vivo from sympathetic nerve endings during marked and rapid increases in sympathetic tone. They suggest a lack of relationship between NA and NPY release. Alpha 2-adrenoceptors are involved in the presynaptic control of NPY release from sympathetic tone. Finally, some antihypertensive drugs (clonidine but not beta-blocking agents) are able to decrease plasma NPY levels.
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PMID:[Neuropeptide Y, orthosympathetic nervous system, hypertension and alpha-2 adrenergic receptors]. 165 47

Neuropeptide Y is colocalized with norepinephrine in both central and peripheral noradrenergic neurons. In this study, we examined the regulatory mechanisms of neuropeptide Y on norepinephrine release in the medulla oblongata of rats. Neuropeptide Y inhibited the stimulation-evoked [3H]norepinephrine release in a dose-dependent manner in slices of medulla oblongata of Sprague-Dawley rats (1 Hz, S2/S1 ratio, control, 0.946 +/- 0.040 [+/- SEM], n = 6; neuropeptide Y 1 x 10(-8) M, 0.676 +/- 0.022, n = 6, p less than 0.05; neuropeptide Y 1 x 10(-7) M, 0.589 +/- 0.014, n = 6, p less than 0.05). Neuropeptide Y potentiated inhibition of [3H]norepinephrine release by the alpha 2-agonists UK 14,304 and clonidine. The blockade of alpha 2-adrenergic receptors by RX 781,094 diminished inhibitory effects of neuropeptide Y on norepinephrine release. Pretreatment of pertussis toxin (a toxin that interferes with the coupling of inhibitory receptors to adenylate cyclase) attenuated the suppression of norepinephrine release by neuropeptide Y. In spontaneously hypertensive rats, the inhibitory effect of UK 14,304 and neuropeptide Y on norepinephrine release from the medulla oblongata was significantly less than in age-matched Wistar-Kyoto rats. These results show that neuropeptide Y inhibits norepinephrine release partially mediated by alpha 2-adrenergic receptors and the pertussis toxin-sensitive guanosine triphosphate-binding proteins in rat medulla oblongata. Furthermore, less suppression of norepinephrine release by UK 14,304 and neuropeptide Y in spontaneously hypertensive rats suggests that alpha 2-adrenergic receptors and neuropeptide Y might be involved in the regulation of central sympathetic tone in hypertension.
Hypertension 1990 Jun
PMID:Norepinephrine release and neuropeptide Y in medulla oblongata of spontaneously hypertensive rats. 197 38

Plasma levels of chromogranin A + B, neuropeptide Y and catecholamines were analysed before, during and after surgery in seven patients with pheochromocytoma. The aim of the study was to determine the diagnostic sensitivity of these plasma amines and peptides, and to investigate their peroperative fluctuations. Chromogranin A + B in plasma was increased preoperatively in all patients, showed no significant increase during surgery, and normalized postoperatively. Neuropeptide Y, which alone can induce hypertension, was present in high levels in plasma from three patients preoperatively, increased further in four patients during surgery, and was postoperatively low in all patients. Fractionated plasma catecholamines were increased in five patients before surgery, increased in all patients during tumour dissection, and normalized postoperatively. It may be concluded that plasma chromogranin A + B exhibited as high a sensitivity for pheochromocytoma as fractionated urinary catecholamines in the patients studied.
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PMID:Plasma chromogranin A + B, neuropeptide Y and catecholamines in pheochromocytoma patients. 204 Aug 71

Neuropeptide Y is known to enhance blood pressure responsiveness to various constrictors, including angiotensin II, and to suppress renin secretion. This study was undertaken to assess the effect of neuropeptide Y on the development of two-kidney, one clip renal hypertension. Normotensive rats either had a silver clip placed on the left renal artery or were sham-operated upon. An osmotic minipump, which was connected via a catheter to a jugular vein, was implanted subcutaneously in all rats. These pumps delivered either neuropeptide Y (0.001 microgram/min) or saline intravenously. Eight days later, an intra-arterial catheter was inserted and the rats were studied while not anesthetized on the following day. Neuropeptide Y did not affect body weight. In clipped rats, neuropeptide Y prevented the development of hypertension and suppressed renin secretion. Neuropeptide Y significantly decreased blood pressure also in sham-operated rats, although it had no effect on plasma renin activity. These data indicate that prolonged neuropeptide Y infusion may lower blood pressure by different mechanisms, one of which is probably a suppression of renin release.
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PMID:Prevention of renal hypertension in the rat by neuropeptide Y. 215 52

Neuropeptide Y (NPY) is closely associated to stress-reactive structures in the central and peripheral nervous system. In the periphery, the peptide is colocalized with catecholamines in postganglionic sympathetic fibres and the adrenal medulla. In the brain, the paraventricular nucleus of the hypothalamus receives a dense innervation of NPYergic neurons, some of which also contain monoamines. With the use of a specific immunoradiometric assay, we have demonstrated that NPY is released into the peripheral circulation during psychological stress together with catecholamines. The postganglionic origin of the peptide was demonstrated by the activity of the nicotinic antagonist hexamethonium to attenuate the response. Adrenalectomy or insulin-induced hypoglycemia did not alter basal or stimulated NPY plasma levels, showing that the adrenal is not a major source of circulating NPY in the rat. Although NPY and noradrenaline are frequently released in parallel in various experimental conditions, a clear dissociation can be found in several cases, such as cold stress or the response to phentolamine, where no change can be seen in plasma NPY despite a large activation of noradrenergic terminals. Furthermore, the neuropeptide may play a role in stress-induced pathological states such as hypertension, since its release is greater in animals previously submitted to chronic stress and high-sodium diet. On the other hand, its role in the central nervous system control mechanisms of the stress response is far from being clear, but to understand the interaction of NPY we need a better knowledge of the role of noradrenergic neurons in the central control of the adrenocortical axis or sympathetic nervous system activity.
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PMID:Involvement of neuropeptide Y in neuroendocrine stress responses. Central and peripheral studies. 219 12

The distribution and density of nerves containing vasoactive intestinal polypeptide, substance P, and neuropeptide Y around the cerebral and peripheral blood vessels of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) were studied using an indirect immunofluorescence technique. Neonatal sympathectomy of SHRSP with anti-nerve growth factor and guanethidine was also carried out to study the effect of sympathectomy on the distribution of these nerves. Vasoactive intestinal polypeptide nerve density was higher in the veins and superior mesenteric artery of SHRSP than of WKY and lower in the cerebral arteries of SHRSP than of WKY, but no difference was found in the muscular mesenteric arteries. Sympathectomy reduced the density of these nerves in all the peripheral vessels but had little effect on the cerebral arteries. Density of substance P nerves was similar between SHRSP and WKY in the peripheral vessels but higher in the cerebral arteries of WKY than of SHRSP. Sympathectomy reduced the density of these nerves in the peripheral vessels but increased the density in some cerebral arteries of SHRSP. Neuropeptide Y nerve density was higher in the peripheral blood vessels of SHRSP than of WKY, and no difference was found in the cerebral arteries. Sympathectomy almost completely removed these nerves in the peripheral vessels but had no effect on the cerebral arteries. We suggest that some of the differences in nerve density between SHRSP and WKY, especially those in the peripheral blood vessels, may be related to the development of hypertension in the SHRSP.
Hypertension 1988 Feb
PMID:Peptide-containing nerves around blood vessels of stroke-prone spontaneously hypertensive rats. 245 64

The effect of the intrathecal administration of neuropeptide Y (NPY) on blood pressure and heart rate of anesthetized normotensive and hypertensive rats was studied. Neuropeptide Y was observed to produce a decrease in the blood pressure of Sprague-Dawley, Wistar Kyoto (WKY), DOCA-salt, and DOCA-sham control rats. The maximum percent decrease in blood pressure of Sprague-Dawley rats was 12.8 and 15.2% in response to 0.1 and 1.0 nmol NPY, respectively. Similar changes in heart rate were observed. The depressor effect of intrathecal NPY was attenuated by prior treatment with yohimbine and propranolol but not prazosin. The depressor effect of intrathecal NPY observed in normotensive and DOCA-salt hypertensive rats was not seen in the spontaneously hypertensive rat (SHR). The studies extend to the spinal cord the list of regions and tissues where NPY can produce physiological effects. It is concluded that the effects of NPY are closely associated with sympathetic preganglionic neurons in the spinal cord that the depressor effect of NPY involves alpha 2 and beta adrenoceptors, and that a loss of the depressor effect of NPY may contribute to the development or maintenance of hypertension in the SHR.
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PMID:Alterations in blood pressure of normotensive and hypertensive rats following intrathecal injections of neuropeptide Y. 246 49


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