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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Catecholamine and vasopressin content were studied in discrete brain nuclei of the Sabra strain of hypertension prone (SBH) and resistant (SBN) rats. Higher concentrations of dopamine, norepinephrine and epinephrine were observed in the median eminence of SBN compared to SBH or controls (SB) rats. Dopamine and epinephrine levels were higher in the lateral septal nucleus of SBH rats as compared to SBN or SB. Vasopressin content in discrete regions along the hypothalamo-pituitary axis was elevated in both SBH and SBN as compared to SB, but were especially elevated in the SBH group. The catecholamine and vasopressin changes found in SBH are different than those described in other genetically hypertensive rats indicating a difference in either the pathogenesis or central response to hypertension of this strain.
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PMID:Catecholamines and vasopressin in forebrain nuclei of hypertension prone and resistant rats. 732 83

A study was performed to investigate the neurohypophyseal dopaminergic axis in terms of its biosynthetic activity and possible changes associated with spontaneous hypertension (SHR). An in vitro system was used in which isolated neuro-intermediate lobes were incubated with the catecholamine precursor, 3H-tyrosine. Dopamine (DA) content and 3H-DA were monitored using electrochemical detection coupled with high pressure liquid chromatographic separation. A time course study showed that there was significant incorporation of 3H-tyrosine into 3H-DA. In the SHR, both neurohypophyseal DA content and biosynthetic activity were reduced. Tissue levels of 3H-DA decreased from 651 to 297 dpm/posterior pituitary. A test of the effect of dehydration on neurohypophyseal dopaminergic activity revealed that water deprivation (48 hrs) caused an increase in DA biosynthesis in the hypertensive, but not the normotensive animal. This may have been due to a greater stimulation of the neurohypophyseal axis in the SHR since these animals showed significantly higher plasma vasopressin levels and hematocrits in response to dehydration. These results demonstrate that the neurohypophysis contains an active dopaminergic system which is altered in genetic hypertension.
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PMID:Neurohypophyseal dopamine biosynthesis in the spontaneously hypertensive rat. 733 97

Dopamine has been used for many years to treat patients with severe heart failure. It is not clear whether improvements of cardiac function may be due to a direct action on heart. This study was aimed to investigate the direct action of dopamine on failing heart. we chose male Wistar rats which had undergone uninephrectomy under ether anaesthesia to induce hypertension to result in heart failure. After 5 weeks the hearts were excised and perfused according to Langerdoff's technique. Heart rate, systolic and diastolic ventricular pressures, the derivative of the intraventricular pressure time ratio, and coronary flow were measured at baseline, at 2 and 5 min and then every 5 min during a 30-min period. Rat hearts were divided into 4 groups of 5 hearts: group 1, perfused without drug; group 2, perfused with dopamine at 4 micrograms/kg/min; group 3, perfused with dopamine at 8 micrograms/kg/min; group 4, perfused with dopamine at 8 micrograms/kg/min and with 100 nM I.C.I. 118.551 (beta 2-ant: beta-2 receptors antagonist) at the same time. Our results show that dopamine induced a negative inotropic effect and a reduction of coronary flow. Moreover, there was a significant chronotropic action even when dopamine was administered at high concentrations. So we found no positive dopamine effect on isolated failured hearts of rat. This might be explained by both alpha-1-induced vasoconstriction and the stimulation of alpha-1B receptors. We conclude that the favourable effects of dopamine in heart failure could be due to DA1 vasodilation rather than to a direct inotropic action on the heart.
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PMID:Effects of dopamine on isolated failing rat heart. 755 68

Changes in dopamine neurotransmission in the nucleus accumbens of the spontaneously hypertensive rat (SHR) may be involved in the pathogenesis of hypertension. This investigation tested the hypothesis that the sulfated octapeptide cholecystokinin (CCK8S) induced release of dopamine is greater in the SHR than in its normotensive control, the Wistar-Kyoto rat (WKY). Dopamine and its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were sampled using microdialysis in the caudal half of the nucleus accumbens of 10-week-old anesthetized SHRs and WKYs. Samples were collected in the following order: 3 baseline, 3 CCK8S (10 mumol/l), and 3 postdrug samples. The samples were then analyzed using high pressure liquid chromatography with electrochemical detection. CCK8S increased dopamine and DOPAC levels in both the SHR and WKY with a larger increase in basal dopamine in the SHR (greater than 200%). Perfusion of the nucleus accumbens with 1 mumol/l of CCK8S or the nonsulfated form of CCK8 (CCK8US, 10 mumol/l) produced no significant increase in the release of dopamine in the SHR. These results indicate that CCK8S-induced release of dopamine in the nucleus accumbens is greater in the SHR. Changes in CCK8S neurotransmission/receptor function may be responsible for the alterations in dopaminergic function of the SHR and the pathogenesis of hypertension.
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PMID:Cholecystokinin-induced release of dopamine in the nucleus accumbens of the spontaneously hypertensive rat. 758 28

1. To clarify the possible role of tissue catecholamines in the development of hypertension, we investigated the effect of bilateral renal denervation on the catecholamine contents of central and peripheral tissues in spontaneously hypertensive rats (SHR). 2. Norepinephrine (NE) content in renal cortex, renal medulla, and adrenal gland was higher in 7 week old SHR than age-matched Wistar-Kyoto rats (WKY). Dopamine (DA) content in the brainstem and hypothalamus was also higher in SHR, but NE and epinephrine (EPI) content in these areas were not different between strains. Similar differences in catecholamines were observed in 9 week old rats in which a sham operation of bilateral renal denervation was performed 2 weeks previously. 3. Bilateral renal denervation produced an almost complete reduction of NE content in the kidney in both strains and prevented the development of hypertension. DA content in the brainstem was also decreased by renal denervation in SHR but not in WKY. NE and EPI content in central tissues were not affected by renal denervation. 4. These results suggest that DA content in brainstem area, as well as NE content in the kidney, have a relationship in the development of hypertension in SHR.
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PMID:Effect of renal nerve denervation on tissue catecholamine content in spontaneously hypertensive rats. 758 6

Dopamine is an essential and indispensable catecholamine, which acts not only as a neurotransmitter in dopaminergic and noradrenergic sympathetic neurons but also as an autocrine/paracrine substance in non-neuronal tissues. The regulatory mechanism of dopamine synthesis in neuronal tissues seems to be different from that in non-neuronal tissues. Among receptors specifically bound to dopamine, five different receptors have already been cloned. Dopamine exhibits vasodilative and natriuretic effects by stimulating specific dopamine receptors located in renal tubular cells, blood vessels, etc. Physiological effects of dopamine appear to be protective against hypertension and sodium retention. Spontaneously hypertensive rats (SHR) are known to have an enhanced dopamine generation associated with the increased sympathetic nervous activity. A defect of renal D1-receptor-mediated coupling to adenylate cyclase has also been demonstrated in SHR. On the other hand, it has been reported that Dahl salt sensitive rats exhibit defective dopamine synthesis during high salt intake, which may be a definitive abnormality in this strain. The pathophysiological role of peripheral dopamine is essential hypertensive patients is still controversial. Considering the previous studies, it seems to be the case that essential hypertensive patients with increased sympathoadrenergic activity show enhanced dopaminergic discharge where dopamine may negatively modulate high blood pressure, and that stable essential hypertensive patients with salt-sensitivity and/or suppressed renin activity show insufficient dopamine synthesis in the kidney.
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PMID:Recent aspect of the role of peripheral dopamine and its receptors in the pathogenesis of hypertension. 764 68

A defective dopamine DA1 receptor has been suggested to be involved in the salt-sensitive hypertension in Dahl-S rats (DS). To investigate the consequences of this defect, the influence of DA1 receptor blockade (SCH23390) and of dopamine-synthesis inhibition (benserazide) on volume expansion (VE)-induced sodium and dopamine excretion was studied in anesthetized prehypertensive DS and salt-resistant Dahl rats (DR). Under control conditions all measured variables were equal in DR and DS. During VE (5% of BW), sodium and dopamine excretion increased similarly in the two strains. During peak natriuresis mean arterial blood pressure was 119 +/- 3 and 122 +/- 3 mm Hg, respectively. In DR treated with SCH23390, sodium excretion was only 72% of that in vehicle-treated DR. Dopamine excretion increased, however, as in vehicle-treated DR. In DS, treatment with SCH23390 did not attenuate natriuresis and dopamine excretion also increased as in vehicle-treated DS. In benserazide-pretreated DR and DS, sodium excretion during VE was similar, but only 50-51% of that in the respective vehicle-treated group. Dopamine excretion decreased by about 80% in both strains. In conclusion, prehypertensive DR and DS have a similar capacity to acutely excrete an intravenous saline load and to generate dopamine. The total dopamine involvement in VE-induced natriuresis is also comparable in the two strains, but the natriuresis mediated by DA1 receptors is pronounced in DR and non-existent in DS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo evidence for a defect in the dopamine DA1 receptor in the prehypertensive Dahl salt-sensitive rat. 771 39

Dopamine is one of the major natriuretic hormone. It acts as an autocrine or paracrine factor to inhibit Na+ transport in several tubular segments. Na+,K(+)-ATPase is an important target protein for dopamine. Studies of the tubular effects of dopamine have provided new information about the coupling of dopamine to intracellular signaling systems and about the molecular mechanism for dopamine interaction with other hormones. Several lines of evidence now suggest that abnormalities of the renal dopamine system can lead to salt-sensitive hypertension.
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PMID:Dopamine action and metabolism in the kidney. 785 Apr 10

Dopamine is a natriuretic hormone that acts by inhibiting tubular Na+, K(+)-ATPase activity by activation of the dopamine-1 receptor (the thick ascending limb [TAL] of Henle) or by a synergistic effect of dopamine-1 and dopamine-2 receptors (the proximal tubule). The dopamine-1 receptor is coupled to adenylate cyclase. In this article we show that prehypertensive Dahl salt-sensitive (DS) rats have a blunted natriuretic response to dopamine determined during euvolemic conditions compared with Dahl salt-resistant (DR) rats. Furthermore, we have examined the renal tubular effects of dopamine in DS and DR rats. Basal Na+,K(+)-ATPase activity was similar in DS and DR rats. In proximal tubule, dopamine (10(-5) M) inhibited Na+,K(+)-ATPase activity in DR but not in DS rats. The dopamine-2 agonist LY171555 (10(-5) M) together with dibutyryl cyclic AMP (10(-6) M) inhibited proximal tubule Na+,K(+)-ATPase activity in both DS and DR rats. LY171555 alone had no effect. In TAL, the dopamine-1 agonist fenoldopam (10(-5) M) inhibited Na+,K(+)-ATPase activity in DR but not in DS rats. Dibutyryl cyclic AMP (10(-5) M) inhibited TAL Na+,K(+)-ATPase activity in both DS and DR rats. In cell suspensions from the cortex and the medulla, activation of the dopamine-1 receptor significantly increased cyclic AMP content in DR but not in DS rats. The results indicate that DS rats lack the capacity to inhibit tubular Na+,K(+)-ATPase activity because of a defective dopamine-1 receptor adenylate cyclase coupling. This defect may contribute to the impaired natriuretic capacity in DS rats.
Hypertension 1993 Jun
PMID:Dopamine regulation of renal Na+,K(+)-ATPase activity is lacking in Dahl salt-sensitive rats. 809 63

Eleven patients with moderate to severe hypertension were studied at the Vargas Hospital of Caracas. The patients were pretreated with labetalol, 800 to 1200 mg/day, orally, over a period of 1 week, after which an intravenous infusion of dopamine, .5 to 3 micrograms/kg/minute, was given. Two intravenous dopamine infusions (30 minutes each) were performed before and after the injection of metoclopramide (30 mg, intravenous bolus). Two washout periods were also included before and after metoclopramide administration. Dopamine induced a decrease of blood pressure from 171.9 + 6.35/103.6 +/- 3.12 to 152.7 +/- 7.55/93.8 +/- 2.97 mm Hg (P < .001) without altering heart rate, and it increased plasma insulin levels from 8.29 +/- .70 microU/mL to 12.09 +/- 1.83 microU/mL (P < .01). Metoclopramide caused no changes of blood pressure or plasma insulin levels. Hypotensive responses and plasma insulin increases due to dopamine were blocked by metoclopramide, however. The authors conclude that a dopaminergic receptor may be involved in some cardiovascular responses and in modulating insulin secretion in humans.
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PMID:Dopamine-induced antihypertensive effects and plasma insulin rise are blocked by metoclopramide in labetalol-treated patients. 813 57


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