Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aortic rings from SHR are reported to have a decreased relaxation response to the endothelium-dependent agent acetylcholine compared with rings from WKY rats. Thus, a reduced EDRF (nitric oxide) response could contribute to hypertension. We found that in mesenteric small resistance arteries (200 microns I.D.) taken from 5- to 50-week old rats and mounted in a Mulvany-Halpern myograph, that the concentration-response curves to acetylcholine were similar in range and sensitivity (EC50) in arteries from SHR and WKY rats at the same age. Similarly, in small resistance arteries from human buttock skin, the relaxation to acetylcholine was not different between vessels from normotensive volunteers (mean BP = 95.2 +/- 1.5 mm Hg) and patients with untreated essential hypertension (mean BP = 116.5 +/- 2.5 mm Hg). In rabbits with chronic renovascular hypertension (cellophane renal wrap), acetylcholine and adenosine infusions into the lower abdominal aorta caused falls in hindquarter resistance that were enhanced in range, but with no change in sensitivity compared with normotensive rabbits. In normotensive rabbits, nitric oxide synthase inhibition with N omega-nitro-L-arginine infusion caused a rise in blood pressure, fall in hindquarter conductance and blockade of the acetylcholine responses. These experiments suggest that at the level of resistance arteries in vivo and in vitro, a defect in the receptor-stimulated response to EDRF associated with hypertension could not be detected. Apparently, basal nitric oxide is important in resting vasodilator tone, but its role in chronic hypertension is still unclear.
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PMID:Release of endothelium-derived relaxing factor from resistance arteries in hypertension. 137 18

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

The activity of NO-synthase and formation of NO (EDRF) were assessed by an increase in the activity of NO-dependent hyanilate cyclase in response to L-arginine in vitro in platelets of 61 pregnant females (39, 8 14 with essential hypertension, preeclampsia and healthy controls, respectively) and in 9 hypertensive nonpregnant females. Compared to healthy pregnant females, EDRF synthesis activity was inhibited in hypertensive gravidas but enhanced in preeclampsia patients. Effectiveness of exogenic donator NO (transdermal nitroglycerine, Nitroderm NNS 5) was studied in a randomised trial of 76 gravidas with essential hypertension (EH), EH and chronic glomerulonephritis (GN). 39 of them were given transdermal nitroglycerine, 37 received acetylsalicilic acid and curantil. The number of treatment failures was the same in both groups. The conclusion is made that nitro compounds are adequate for use in EH and chronic GN gravidas.
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PMID:[Nitric oxide: its role in the development of pregnancy complications and in their prevention in women with hypertension and chronic glomerulonephritis]. 929 65

It has been proposed repeatedly that essential hypertension as well as secondary hypertension is associated in a causative manner with endothelial dysfunction in the resistance vessels. Endothelial damage and dysfunction may be expected to attenuate the endogenous vasodilator mechanism of EDRF (nitric oxide) and hence cause a rise in blood pressure. This attractive hypothesis, put forward a few years ago, is subject to considerable debate at present. In the present survey the arguments in favour and against this hypothesis are critically discussed. The following arguments support the causative association between endothelial dysfunction: the hypertensive effect of NO-synthase blockade by L-NAME and related agents; the antihypertensive effect of L-arginine in salt-loaded Dahl rats; the impaired vasodilator effect in the forearm vascular bed of hypertensives; diminished NO-synthesis in hypertensives. However, several findings speak against the association between hypertensive disease and endothelial dysfunction. For instance: no clear demonstration of impaired endothelial function in isolated vessels of hypertensive patients and animals; studies in the human forearm vascular bed where endothelial function appears to be fully intact in hypertensives. Attempts are made to explain the discrepancies between the various findings. So far the association between endothelial dysfunction and hypertension appears to be an uncertain one.
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PMID:Endothelial dysfunction in hypertension. A critical evaluation. 949 30

At the opportunity of the 100th anniversary of S. Riva-Rocci's publications on the new sphygmomanometer the author presents a review of the main publications which made this method possible and a review of clinical and pathological studies which led to the recognition of essential hypertension (EHT). He also mentions main adopted criteria of hypertension and draws attention to the difficulties associated with a definition and classification of EHT because of the variations in pressure and differences of "normal" values in various populations. From multicentre intervention studies precise and generally valid criteria for individual treatment cannot be derived. As to recent of work on the pathogenesis of EHT the author draws attention to the importance of endothelin and NO (EDRF), which play a part in the genesis of changes in the vascular wall in atheromatosis and also in hypertension. A new discovery is the bond between NO and haemoglobin (S-nitrosohaemoglobin). In addition to proved and located genetic factors also external factors are involved, in particular psychosocial factors, diet, body weight, smoking etc. on which prevention and treatment must be focused. Medicamentous treatment markedly improves the prognosis of hypertension. Antihypertensive drugs from all main groups of drugs are used. Dosage still remains an open question which cannot be resolved completely on the basis of intervention trials. ACE-inhibitors hold an important place--they reduce the blood pressure and also prevent progression of left ventricular hypertrophy. Beta-blockers and diuretics still remain the basis of first line treatment. Among Ca-inhibitor, preparation with long-term action are preferred. Open questions include--apart from dosage--the comparison of the efficacy/side effects ratio of new effective drugs (A I, A II, renin) and older antihypertensive drugs when used on a long-term basis; furthermore the justification to administer vasodilatating drugs as monotherapy and in combinations during long-term treatment with regard to the activation of the sympathetic nerve and risk of hypotension. The author discusses the sympathetic activation to which BP should be reduced and thus also the question of doses reduction and discontinuation of the drug--in particular in old patients. And finally, the role of hypertension as the sole cause of increased mortality (EEHT per se) must be proved. In practice the problems of the detection rate, adherence, information and correct treatment are of major importance.
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PMID:[100 years of hypertension]. 951 Dec 69

In retrospect, basic research in the fields of NO and cyclic GMP during the past two decades appears to have followed a logical course beginning with the findings that NO and cyclic GMP are vascular smooth muscle relaxants, that nitroglycerin relaxes smooth muscle by metabolism to NO, progressing to the discovery that mammalian cells synthesize NO, and finally the revelation that NO is a neurotransmitter mediating vasodilation in specialized vascular beds. A great deal of basic and clinical research on the physiological and pathophysiological roles of NO in cardiovascular function has been conducted since the discovery that EDRF is NO. The new knowledge on NO should enable investigators in this field to develop novel and more effective therapeutic strategies for the prevention, diagnosis and treatment of numerous cardiovascular disorders. Since NO elicits a protective and beneficial action in many disease states, novel NO donor drugs for clinical use should prove to be very effective drugs for the treatment of essential hypertension, stroke, coronary artery disease, vascular complications of diabetes, impotency and other disorders involving the vascular system.
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PMID:Nitric oxide as a unique signaling molecule in the vascular system: a historical overview. 1251 88

We reported impaired endothelium-derived relaxation factor/nitric oxide (EDRF/NO) responses and constitutive nitric oxide synthase (cNOS) activity in subcutaneous vessels dissected from patients with essential hypertension (n = 9) compared with normal controls (n = 10). We now test the hypothesis that the patients in this study have increased circulating levels of the cNOS inhibitor, asymmetric dimethylarginine (ADMA), or the lipid peroxidation product of linoleic acid, 13-hydroxyoctadecadienoic acid (HODE), which is a marker of reactive oxygen species. Patients had significantly (P < 0.001) elevated (means +/- SD) plasma levels of ADMA (P(ADMA), 766 +/- 217 vs. 393 +/- 57 nmol/l) and symmetric dimethylarginine (P(SDMA): 644 +/- 140 vs. 399 +/- 70 nmol/l) but similar levels of L-arginine accompanied by significantly (P < 0.015) increased rates of renal ADMA excretion (21 +/- 9 vs. 14 +/- 5 nmol/mumol creatinine) and decreased rates of renal ADMA clearance (18 +/- 3 vs. 28 +/- 5 ml/min). They had significantly increased plasma levels of HODE (P(HODE): 309 +/- 30 vs. 226 +/- 24 nmol/l) and renal HODE excretion (433 +/- 93 vs. 299 +/- 67 nmol/micromol creatinine). For the combined group of normal and hypertensive subjects, the individual values for plasma levels of ADMA and HODE were both significantly (P < 0.001) and inversely correlated with microvascular EDRF/NO and positively correlated with mean blood pressure. In conclusion, elevated levels of ADMA and oxidative stress in a group of hypertensive patients could contribute to the associated microvascular endothelial dysfunction and elevated blood pressure.
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PMID:Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension. 1868 64