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)

The effects of ovine corticotropin releasing factor (o-CRF) on plasma aldosterone, 18-OH-corticosterone (18-OHB), plasma adrenocorticotropin (ACTH) and cortisol were determined in eight patients with primary aldosteronism, six with aldosterone-producing adenoma (APA) and two with idiopathic hyperaldosteronism (IHA). The results were compared with those in six normal subjects and eleven patients with essential hypertension (EHT, 5 with low renin and 6 with normal renin). In patients with APA, the peak plasma aldosterone and 18-OHB responses to 100 micrograms iv of o-CRF (226% and 113% increase from baseline, respectively) were greater than those in EHT and normal subjects. The net integrated aldosterone and 18-OHB responses (840 +/- 156, and 419 +/- 121 ng/dl.hr, respectively) were also significantly greater (p less than 0.01) in APA than those in normals and EHT. In two patients with IHA, both the peak and net integrated aldosterone response were smaller than those in APA, in spite of nearly identical plasma ACTH and cortisol responses. These results suggest that augmented responses of mineralocorticoids to o-CRF may be characteristic of aldosteronism due to APA, mediated by CRF-induced ACTH, and possibly other proopiomelanocortin (POMC)-derived peptides.
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PMID:Effects of corticotropin-releasing factor (CRF) on aldosterone and 18-hydroxycorticosterone in essential hypertension and primary aldosteronism. 283 82

The acute effect on the renin-angiotensin system and the pharmacokinetic properties of delapril, a new angiotensin converting enzyme inhibitor and its active diacid metabolites (delapril diacid and 5-hydroxy delapril diacid) arising from delapril in vivo were investigated in 4 hypertensive patients with chronic renal failure (CRF: 4 males, average age 49.5 (37-64) years, mean Ccr 22.2 ml/min/1.73 m2) and 9 patients with essential hypertension (EH: 6 males, 3 females, average age 42.8 (28-61) years, mean Ccr 79.3 ml/min/1.73 m2). In CRF, following a single dose of delapril hydrochloride (30 mg), the biological half lives (t1/2) of delapril diacid and 5-OH-delapril diacid were 4.69, 12.88 hours, the maximum serum concentration (Cmax) and the area under the plasma concentration-time curve ([AUC]24(0)) of delapril and its diacid metabolites were 414, 797 and 435 ng/ml, and 658, 6400 and 5068 ng X h/ml, respectively. In EH, the t1/2 of delapril diacid and 5-OH-delapril diacid were 1.21, 1.40 hours and the Cmax and [AUC]24(0) of delapril and its diacid metabolites were 489, 635 and 229 ng/ml, and 572, 1859 and 948 ng X h/ml, respectively. The [AUC]24(0) in CRF were significantly increased as compared with those in EH. The cumulative urinary excretions were significantly lower in CRF than in EH. The serum angiotensin converting enzyme (ACE) was markedly inhibited in both groups up to 24 hours. The plasma concentration of angiotensin II decreased in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacokinetics and acute effect on the renin-angiotensin system of delapril in patients with chronic renal failure. 303 May 95

Effects of captopril on arterial pressure (AP) and renal function were investigated in patients with non-malignant "benign" or malignant phase essential hypertension (EH group), or with chronic renal failure (CRF group). After captopril administration, AP and renal vascular resistance (RVR) decreased significantly, and renal blood flow (RBF) and plasma renin activity (PRA) increased in both groups. Glomerular filtration rate (GFR) increased in the EH group, but was unchanged in CRF. Filtration fraction decreased in the malignant hypertension and CRF groups. Significant correlations were found between baseline PRA and baseline RVR, and the captopril-induced decrease in mean AP, decrease in RVR, increase in RBF, and increase in GFR in the EH group, while these associations were not observed in CRF. These results indicate that the high AP, RVR, suppressed RBF and GFR in the EH group were closely related to activity of the renin-angiotensin system, but not so the low RBF and GFR in CRF. Small doses of captopril may improve impaired renal function in EH, and may not cause deterioration in the CRF group.
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PMID:Renal haemodynamics and comparative effects of captopril in patients with benign- or malignant-essential hypertension, or with chronic renal failure. 330 Oct 82

The present study describes the relationship between the whole blood Pb, plasma Al and plasma V levels and the arterial hypertension, for four groups of individuals: 20 normotensive azotemic patients in periodic hemodialysis (CRF), 20 hypertensive azotemic patients in periodic hemodialysis (CRF-AHT), 20 individuals with severe essential hypertension and normal renal function (AHT) and 20 individuals with normal renal function and normal blood pressure (controls) evaluated during a period of 1 year. The renal population's blood Pb was comparable with that found in the non-renal groups. Blood Pb in the essential AHT was higher than in controls (P < 0.05). CRF and CRF-AHT showed higher Al levels than those individuals with normal renal function (P < 0.01). In CRF, plasma Al did not correlate with the arterial hypertension. Plasma Al was increased in the AHT individuals (P < 0.05) with respect to the control group, suggesting the possible influence of this metal in the appearance of the arterial hypertension. In this study, the CRF-AHT patients had plasma V statistically higher (P < 0.005) than controls. However, no differences were found between plasma V of CRF and CRF-AHT groups or between AHT and controls. These results suggest that V in AHT is of doubtful significance, except maybe when the renal failure and the arterial hypertension appear together. In summary, high levels of blood Pb and plasma Al are associated with arterial hypertension in individuals without renal disease. Higher plasma V levels were not found in hypertensives with normal renal function with respect to controls.
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PMID:The influence of the blood levels of lead, aluminum and vanadium upon the arterial hypertension. 775 2

For several decades clinicians and researchers have come to recognize the crucial role played by the kidney in the control of blood pressure. Richard Bright in the past had noted that patients with chronic kidney disease often showed evidence of left ventricular hypertrophy and arteriosclerosis. Fredrick Mohamed and Sir William Gull later demonstrated that elevation of blood pressure might occur even in patients with no evidence of kidney disease. There are now hypotheses to support the fact that even primary hypertension has its origin in the kidney. The consequence of hypertension of the kidney is chronic renal failure; Prevalence rates of CRF range from 25 -100 per 100,000 populations and the incidence continues to grow increasingly at a rate of about 8-10% per year thereby posing a major public health problem especially in the developing countries. Management of chronic renal diseases is tedious and very costly. The consequence of the association between kidney and hypertension on the patient, the family, the national economy of a country and the society at large is considerable, hence the need to evolve preventive strategies.
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PMID:The relationship between kidney and hypertension: a review. 1675 61

In normal conditions, the temporal organization of blood pressure (BP) is mainly controlled by neuroendocrine mechanisms. Above all, the monoaminergic systems (including variations in activity of the autonomous nervous system, and in secretion of biogenic amines) appear to integrate the major driving factors of temporal variability, but evidence is available also for a role of the hypothalamic-pituitary-adrenal, hypothalamic-pituitary-thyroid, opioid, renin-angiotensin-aldosterone, and endothelial systems, as well as other vasoactive peptides. Many hormones with established actions on the cardiovascular system (arginine vasopressin, vasoactive intestinal peptide, melatonin, somatotropin, insulin, steroids, serotonin, CRF, ACTH, TRH, endogenous opioids, and prostaglandin E2) are also involved in sleep induction or arousal, which in turn affects BP regulation. Hence, physical, mental, and pathological stimuli which may drive activation or inhibition of these neuroendocrine effectors of biological rhythmicity, may also interfere with the temporal BP structure. On the other hand, the immediate adaptation of the exogenous components of BP rhythms to the demands of the environment are modulated by the circadian-time-dependent responsiveness of the biological oscillators and their neuroendocrine effectors. These notions may contribute to a better understanding of the pathophysiology and therapeutics of hypertension, myocardial ischemia and infarction, cardiac arrhythmias and all kind of acute cardiovascular accidents. For instance, the normal temporal balance between external stimuli and neurohumoral influences with endogenous rhythmicity is preserved in uncomplicated, essential hypertension, whereas it is frequently lost in complicated and secondary forms of hypertension where gross alterations are found in the circadian profile of BP. When all the gates of the critical physiologic functions are aligned at the same time, the susceptibility, and thus risk, of adverse events becomes extremely high, even in the presence of minor environmental stimuli that could be usually harmless, and circadian rhythms of cardiovascular events are observed. This implies that one cannot afford to miss what happens during day but also night. Moreover, the requirement for preventive and therapeutic interventions varies predictably during the 24 h, suggesting that the delivery of protective or preventive medications should be synchronized in time in proportion to need, as determined by established rhythmic patterns in cardiovascular function as well as risk, in a manner that will avert or minimize their undesired side effects.
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PMID:The circadian organization of the cardiovascular system in health and disease. 2485