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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to investigate whether some relation exists between afferent arteriolar resistance (AAR) and the renal production of nitric oxide (NO) and prostacyclin (PGI2) in 21 patients with untreated essential hypertension and 20 normotensive controls. All subjects were studied in conditions of an unlimited Na+ diet both basally and after a four-hour amino acid infusion. AAR was calculated using Gomez's equations. Renal production of NO and PGI2 were assessed by radioimmunoassay of the urinary excretion of cGMP and 6-keto-PGF1 alpha, respectively. Baseline AAR was higher (P < 0.01) in hypertensives than in normotensives. The baseline urinary excretion of 6-keto-PGF1 alpha and cGMP were similar in the two groups of subjects. AAR diminished (P < 0.005) in normotensives and remained unchanged in hypertensives after amino acid infusion. Urinary excretion of 6-keto-PGF1 alpha was increased similarly in the two groups of subjects after infusion. Urinary excretion of cGMP remained unchanged in normotensives and decreased by 31% in hypertensives after infusion. These findings suggest that afferent vasoconstriction present in hypertensive patients is unresponsive to the vasodilatory manoeuvre of amino acid infusion. This lack of response may be due to a defective renal synthesis of NO in these patients.
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PMID:Vasoconstriction of the afferent arteriole and defective renal synthesis of nitric oxide in essential hypertension. 874 33

The endothelium plays a very important role in the regulation of vascular function by way of its barrier role, by interaction with circulating cells such as platelets, which may release vasoactive or growth regulating agents, and through production of substances which modulate vascular tone and smooth muscle cell growth, and which may also exert antithrombotic effects. The endothelium of resistance arteries, vessels critically involved in generating resistance to flow and which play an important role in hypertension, has been studied mainly from the point of view of generation of agents which regulate vascular tone and growth. Endothelium-derived relaxing factors such as nitric oxide, prostacyclin, hyperpolarizing factors (EDHF) and possibly C-type natriuretic peptide (CNP), are counteracted by endothelium-derived contracting factors, which include endothelins and contracting factors (EDCF) which are less well characterized and appear to be cyclooxygenase products. In experimental hypertension in animals, and in human essential hypertension, these mechanisms may be altered. There may be a reduced generation of endothelium-derived nitric oxide and enhanced production of EDCF. Some of the mechanisms involved in the role these agents play in the physiology of resistance arteries and pathologically in hypertension will be reviewed.
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PMID:The endothelium of resistance arteries: physiology and role in hypertension. 899 88

The major antihypertensive effect of losartan, a nonpeptide angiotensin II antagonist, is thought to be due to inhibition of the pressor effects of angiotensin II. It is possible, however, that losartan alters the synthesis of vasodilator or vasoconstrictor prostaglandins (PG), thus contributing to its antihypertensive effect. Sixteen postmenopausal women with essential hypertension, with a mean age of 59 years and diastolic blood pressures of 95 to 115 mm Hg, were enrolled in a 12-week, single-blind study to determine the effects of losartan on blood pressure, renal and extrarenal PG production, plasma renin activity (PRA), plasma aldosterone, and routine biochemical parameters. The subjects received placebo during weeks 1 to 4, 50 mg losartan daily during weeks 5 to 8, and placebo during weeks 9 to 12. During the 4-week treatment period, there were no significant, sustained changes in renal or extrarenal synthesis of PGE2, PGI2, or thromboxane A2. Losartan significantly reduced systolic blood pressure from 155 +/- 11 mm Hg (mean +/- SD) to 139 +/- 13 mm Hg (P = .001) and diastolic blood pressure from 100 +/- 2 mm Hg to 87 +/- 5 mm Hg (P < .001) despite the fact that the majority of patients had low PRA. Plasma aldosterone concentration decreased from 9.7 +/- 6.5 ng/dL to 5.1 +/- 3.9 ng/dL (P = .002) and serum uric acid declined from 4.6 +/- 0.8 mg/dL to 4.2 +/- 0.8 mg/dL (P = .018) after 4 weeks of treatment with losartan. We conclude that 1) losartan decreases blood pressure in women with essential hypertension and low plasma renin activity; 2) the antihypertensive effect is not associated with sustained changes in renal or extrarenal PG production; and 3) losartan reduces plasma aldosterone and serum uric acid concentrations in patients with essential hypertension.
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PMID:The effects of angiotensin II receptor blockade with losartan on systemic blood pressure and renal and extrarenal prostaglandin synthesis in women with essential hypertension. 899 51

The risk factors of stroke in young adults and in the whole population are the same in general, but there are some special risk factors in young adults. They are congenital or early acquired diseases which are complicating with early stroke. We studied the risk factors of cerebrovascular insults in 150 patients, 20-49 years old (Table 1). This was 26.04 percent of all patients that were hospitally treated in the urgent neurological department over one year. However, twenty years ago, this percent was 20.20 [2]. We found that arterial hypertension was dominant both among young adults (47.99 percent) and in the whole population (Table 2) [1-3]. Essential hypertension was the most frequent, and renal and thyreotoxical hypertensions were rare. The atherogenic level of low density and high density lipoproteins (LDL/HDL) was present in 14.66 percent of young adult patients [3]. Diabetes mellitus, a known risk factor of stroke, was found in 5.33 percent of our studied patients, especially in the juvenile form [1-3]. Besides juvenile diabetes mellitus, we found other risk factors that were characteristic of young adults: systemic lupus erythematosus (3.33 percent), which began at an early vital age, and numerous cerebrovascular complications appeared during the first five years of illness [7]. In this group of young adults, we found no other type of vasculitis, which also can be a risk factor of stroke. Great risk factors of stroke in young adults were arterial-venous malformation, brain aneurysm and congenital muscular hypoplasia of the carotide and middle caliber cerebral arteries-multiple progressive intracranial arterial occlusion or Nishimoto Takeuchi disease or Moya Moya disease, which were found in 3.99 percent of our patients. These diseases were complicated by cerebrovascular haemorrhagic or ischaemic insults over the young vital period [9]. The similar was with congenital or early acquired (rheumatic fever) heart valve defects (3.99 percent in our group), with early cerebrovascular complications due to cardiogenic thromboembolism mechanisms [10]. In 2 percent of patients the stroke was the consequence of anticoagulant therapy. These were the patients with operated heart valve defects (haemodynamic risk factor was eliminated, but haemorrheological risk factor was evident) [2, 3]. Also, disturbances of cardiac rhythm were risk factors of stroke in 2 percent of our patients. The mechanism of stroke originated is cardiogenic thromboembolism or global hypotension and the following ischaemia in the border brain zone [11]. All these risk factors were present in a relatively small number of patients, but they were "strong" risk factors of stroke, especially in young adults. On the other hand, there were nicotinism, alcoholism and obesity. They were present in a greater percent (25.33; 15.66; 18.66 percent), but their influence was slow and indirect by haemorrheologic mechanism (the increasing aggregation of platelets, reduced flexibility of red and white blood cells, changed prostacycline-prostaglandin relation in endothelial and blood cells, viscosity of blood, LDL/HDL) [2, 3, 12, 13]. A prolonged psychogenic stress (8.66 percent in our group) was, also, a risk factor of stroke. It induced increase in catecholamine level, arterial hypertension, constriction of blood vessels, endothelial cell damages, increased aggregation of platelets, changed prostacycline-prostaglandin relation, metabolism of lipids and polysaccharides) [2, 3]. We found no abuse of ephedrine [16] or cocaine [15] as risk factors of stroke in our group, although it was described in litterature. Also, we found no postoperative thromboemolism (foramen ovale apertum). Ischaemic cerebrovascular insults dominated (77.34 percent) in our group of patients. In one article (Canada) [17] haemorrhagic insults were dominant in young adults. In our opinion, the number of our patients was not adequated, as haemorrhagic stroke is also treated in neurosurgical departments. The mor
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PMID:[Risk factors for stroke in young people]. 910 54

For about 120 years we have been looking for the 'cause' of essential hypertension. It is possible that we have merely been wandering through its graveyard, looking at the pathogenetic mechanisms but never the actual cause? Here we pass the gravestone of increased sympathetic activity; there the gravestone of low renin activity. Here high endothelin; there low EDRF. Here high thromboxane A2; there low prostacyclin. It is possible that all these and so many other pathogenetic factors are all due to one basic defect? Is it possible that, in the dead of night while patients with EH have been sleeping, the villain has been lurking in their mouths, stuck somewhere at the back of their throats, hidden from view yet choking them hundreds of times a night. But this intermittent strangulation has not occurred silently. On the contrary, it has made its presence felt in the most irritating way, with snores, groans, grunts, gasps and frightening periods of total apnea. But we, their physicians, never asked about these symptoms, or, if we did, we never paid heed to them. This is clear from the fact that, most cases of OSA occur in association with EH yet are not diagnosed. Perhaps the next 'arousal response' should be the arousal of physicians' consciousness so that they can at long last wake up to the existence of the close connection between sleep-related breathing disorders and hypertension and breathe some new life into the treatment of two old diseases-essential hypertension and secondary hypertension. Early diagnosis and treatment of the sleep-related breathing disorders may not only make the patient feel much better, (something our antihypertensive medications do not always do), but may reduce the blood pressure and prevent the progression of renal and cardiovascular damage as well.
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PMID:Sleep-related breathing disturbances: their pathogenesis and potential interest to the nephrologist. 914 Sep 93

Cicletanine is a new antihypertensive drug that seems to stimulate the synthesis of prostaglandin (PG) I2. However, there is little evidence that cicletanine increases the level of PGI2 in the systemic blood of human subjects long-term. To investigate the antihypertensive mechanism of cicletanine, we measured serially the systemic blood pressure and the levels of both 6-keto-PGF1alpha (a stable metabolite of PGI2) and PGE2 in plasma and urine after administration of cicletanine. Nine patients with essential hypertension on a diet with sodium intake of 120 mEq/day took 100 mg of the drug orally daily every day for 1 week. Systemic blood pressure was measured hourly for 24 h on day 7 of the control period and on days 1 and 7 of the cicletanine period. The two PGs of interest were extracted, purified by high pressure liquid chromatography, and measured by radioimmunoassay. Cicletanine decreased blood pressure without reflexial tachycardia. The plasma levels of 6-keto-PGF1alpha were slightly, but significantly, higher at 3 h after the administration of cicletanine on both days 1 and 7 of administration (on day 1, 3.88 +/- 1.44 pg/mL and on day 7, 4.07 +/- 0.76, means +/- SD, both P < .05 v before administration on day 1) than before administration on day 1 (3.21 +/- 1.25 pg/mL). Plasma PGE2 was higher before and at 3 h after administration on day 7 than at 12 noon on day 7 of the control period. Cicletanine increased the urinary excretion of the two PGs; the increased PG levels partly account for the increased natriuresis in the first 3 days. The antihypertensive effects of cicletanine taken for 1 week were based on natriuresis caused by increased systemic synthesis of the vasodilator PGI2 and partly by the increased renal synthesis of PGI2 and PGE2.
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PMID:Effects of cicletanine on prostaglandin I2 and E2 levels in patients with essential hypertension. 923 29

The endothelium modulates the tone of the underlying vascular smooth muscle by releasing relaxing factors, including prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF). In most types of hypertension, endothelium-dependent relaxations are impaired because of a reduced production and/or action of endothelium-derived NO and EDHF. In essential hypertension, endothelium-dependent relaxations are reduced because of a concomitant release of vasoconstrictor prostanoids (endoperoxides and thromboxane A2). These prostanoids may be produced in the vascular smooth muscle rather than in the endothelium. The endothelial dysfunction observed in hypertension is likely to be a consequence rather than a cause of the disease, representing premature aging of the blood vessels due to the chronic exposure to the high blood pressure. The endothelial dysfunction can be improved by antihypertensive therapy, favoring the prevention of the occurrence of vascular complications in hypertension.
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PMID:Endothelial dysfunction in hypertension. 973 Jan 43

Several mechanisms other than the inhibition of systemic and local formation of angiotensin II (Ang II) have been proposed to play a role in mediating the hypotensive effects of angiotensin-converting enzyme (ACE) inhibitors. In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3',5'-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension. Plasma NO levels were measured by the Griess method after conversion of nitrate to nitrite. Long-term lisinopril treatment significantly reduced blood pressure and increased plasma NO and 6-keto PGF1alpha. The treatment also tended to increase plasma levels of bradykinin and cGMP, but not to a significant extent. The posttreatment NO level was inversely correlated with posttreatment systolic, diastolic, and mean blood pressure (n = 17, r= -.68, P< .01, n = 17, r= -.54, P < .05, and n = 17, r= -.66, P< .01, respectively). The posttreatment bradykinin level was also modestly correlated with posttreatment systolic and mean blood pressure (n = 17, r = -.51, P < .05 and n = 17, r = -.55, P < .05, respectively). In contrast, posttreatment 6-keto PGF1alpha and cGMP levels were not correlated with posttreatment systolic, diastolic, or mean blood pressure. These findings raise the possibility that increased formation of NO and bradykinin, as well as inhibition of the renin-angiotensin system, contribute to the hypotensive effect of the ACE inhibitor observed in our hypertensive patients.
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PMID:Plasma levels of nitric oxide and related vasoactive factors following long-term treatment with angiotensin-converting enzyme inhibitor in patients with essential hypertension. 1053 87

Endothelial cells release both relaxing and contracting factors that modulate vascular smooth muscle tone and also participate in the pathophysiology of essential hypertension. Endothelium-dependent vasodilation is regulated primarily by nitric oxide but also by an unidentified endothelium-derived hyperpolarizing factor and by prostacyclin. Endothelium-derived contracting factors include endothelin-1, vasoconscrictor prostanoids, angiotensin II and superoxide anions. Under physiological conditions, there is a balanced release of relaxing and contracting factors. The balance can be altered in cardiovascular diseases such as hypertension, atherosclerosis, diabetes and other conditions, thereby contributing to further progression of vascular and end-organ damage. In particular, endothelial dysfunction leading to decreased bioavailability of nitric oxide impairs endothelium-dependent vasodilation in patients with essential hypertension and may also be a determinant for the premature development of atherosclerosis. Different mechanisms of reduced nitric oxide activity have been shown both in hypertensive states and several cardiovascular diseases, and endothelial dysfunction is likely to occur prior to vascular dysfunction. Thus, the strategies currently used to improve endothelial dysfunction may result in decreased morbidity and mortality in hypertensive patients.
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PMID:Endothelial dysfunction in hypertension. 1104 Nov 20

An impaired synthesis of prostacyclin has been implicated in the development of essential hypertension (EH). We therefore investigated whether there is an association between the prostacyclin synthase (PGIS) gene and EH using a variable number of tandem repeats (VNTR) polymorphism in the promoter region that influences transcriptional activity of this gene. A total of 125 patients with EH and 125 age-matched subjects with normal blood pressure were studied. The number of VNTR of the five alleles ranged from 3 to 7 repeats in the 250 unrelated Japanese subjects. The allele frequency distribution in the two groups were not significantly different. Thus, this VNTR polymorphism in the PGIS gene is not associated with EH.
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PMID:Polymorphism of the promoter region of prostacyclin synthase gene is not related to essential hypertension. 1136 58


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