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

In order to test the hypothesis that the activity of cardiovascular centres is determined by their content of cAMP a number of drugs which influence the activity of either phosphodiestase or adenylcyclase were injected in doses of 100-1000 mug/kg into the lateral cerebral ventricle of cats. The effects on blood pressure and heart rate were studied. The phosphodiesterase inhibitors papaverine, carbocromene, theophylline and caffeine caused hypertension and tachycardia which increased with the dose while the phosphodiesterase activator imidazole exerted opposite effects. Sodium fluoride which activates adenylcyclase increased blood pressure and heart rate substantially. The results confirm the above-mentioned hypothesis.
 ...
PMID:Further evidence for the involvement of cAMP in central blood pressure regulation. 18 30

Analgesic abuse is a major public health hazard in Australia, and analgesic nephropathy with consequent terminal renal failure is the underlying cause in 20% of the patients requiring dialysis and transplantation. Analgesics are invariably taken in the form of compounds and mixtures. In the aspirin-phenacetin-caffeine (APC) mixture, aspirin appears to be the major nephrotoxic agent and phenacetin appears to play a secondary and synergistic role. The renal disease associated with abuse of analgesics is characteristic and is part of a much wider clinical syndrome, the analgesic syndrome, which includes peptic ulcer disease (35%), anemia (60 to 90%), hypertension (15 to 70%), ischemic heart disease (35%), psychological and psychiatric manifestations, pigmentation, and possible gonadal- and pregnancy-related effects. The primary lesion in analgesic nephropathy is renal papillary necrosis (RPN), and this is a nephrotoxic effect common to all nonsteroid antiinflammatory agents. The most important factor in the management of patients with analgesic nephropathy is the cessation of analgesic abuse, and this leads to improvement and stabilization of renal function. A small proportion of patients will, however, deteriorate in relation to accelerated hypertension, persistent proteinuria, ischemic heart disease, and complications leading to nephrectomy. Patients with analgesic nephropathy are poor risk patients and have a poor prognosis, even after dialysis and transplantation.
 ...
PMID:Analgesic nephropathy: etiology, clinical syndrome, and clinicopathologic correlations in Australia. 36 34

Coffee as a rule develops stimulating effects on the central nervous system, heart and circulation which are mainly caused by caffeine. In certain cases coffee may also have a sedative effect and sometimes even it is useful to fall asleep quickly. Furthermore coffee may be advantageous in the treatment of some functional disorders caused by lacking of dopamine, because coffee is able to increase the dopamine formation in brain. Concerning the effects of coffee in the gastrointestinal-tract and liver-bile system caffeine is only of secondary importance. Hereby certain roasting substances, possibly also chlorogenic acid or caffeic acid should be responsible for the stimulating effects observed in these organs. These stimulating effects could be caused whether directly or indirect e.g. by liberating gastrin or other gastrointestinal hormones. Vitamin niacin, which is formed in greater amounts from trigonelline during the roasting process, may also be important from the nutritional standpoint. Therefore coffee may be prescribed as a true drug in cases of deficiency in vitamin niacin or also in the pellagra disease. By extensive epidemiological studies performed lately it could be demonstrated that there exists no correlation between coffee consumption and certain risk factors as hypertension, heart infarction, diabetes, gout or cancer diseases. Furthermore there was no evidence that coffee or its caffeine content are able to induce genetic alterations or even malformations.
 ...
PMID:[Coffee and health]. 60 27

Hostility, as measured by the Cook-Medley Hostility Scale of the Minnesota Multiphasic Personality Inventory, has been found to predict higher rates of both coronary heart disease and all-cause mortality. To evaluate one mechanism whereby hostility might contribute to health problems, the authors used regression models to determine whether hostility measured in college (1964-1966) predicted coronary risk factors assessed 21-23 years later (1987-1990) in 4,710 men and women. Of this group, 828 had lipids measured (1988-1991). Persons with higher hostility scores in college were significantly more likely at follow-up to consume more caffeine (r = 0.043), to have a larger body mass index (r = 0.055), to have higher lipid ratios (r = 0.092), and to be current smokers (r = 0.069) than those with lower hostility scores during college. Cross-sectional analyses found significant associations of contemporaneous hostility scores with the same four risk factors, as well as with alcohol consumption and hypertension (rs ranging from 0.043 to 0.117). These associations are large enough to have possible public health significance. We conclude that hostility may contribute to health problems through its influences on several coronary risk factors across the adult life span.
 ...
PMID:Hostility during late adolescence predicts coronary risk factors at mid-life. 141 38

Previous studies demonstrate that chronic administration of caffeine causes glomerular filtration to deteriorate in rats with high-renin renovascular hypertension. A partial explanation for these findings could be that chronic administration of caffeine alters the effects of angiotensin II on the kidney. As an initial test of this hypothesis, we compared the acute effects of intrarenal infusions of angiotensin II (3 ng/min) on renal function in control rats versus rats treated with 0.1% caffeine in their drinking water for 1 week. The renal responses to angiotensin II in a group of animals receiving acute intrarenal infusions of adenosine (10 micrograms/min) were also measured to determine whether caffeine and adenosine modulated renal responses to angiotensin II in opposite directions. All studies were performed in the in situ blood perfused rat kidney. Neither caffeine nor adenosine significantly altered angiotensin II-induced changes in renal blood flow, urinary excretory function or renin release. However, caffeine augmented and adenosine attenuated the increase in filtration fraction caused by angiotensin II. The fact that caffeine potentiates angiotensin II-induced increases in filtration fraction without affecting angiotensin II-induced reductions in renal blood flow is consistent with, but does not prove, the hypothesis that chronic administration of caffeine modifies the effects of angiotensin II on the renal microvasculature. If this inference is correct, caffeine could facilitate renal damage in high-renin hypertension by exacerbating angiotensin II-induced increases in glomerular capillary hydrostatic pressure.
 ...
PMID:Effects of chronic treatment with caffeine on kidney responses to angiotensin II. 142 65

1. The cardiovascular effects of the proprietary cold remedies, Mu-cron and Boots Cold Relief tablets were compared with 'placebo' Boots Pain Relief tablets in a double-blind study involving 16 healthy volunteers. Measurements (impedance cardiography, forearm plethysmography) were made over 4 h after oral drug administration. 2. Two Mu-cron tablets (containing phenylpropanolamine [(1R,2S)- plus (1S,2R)-norephedrine] 50 mg) increased blood pressure (maximal effect 18 +/- 1/8 +/- 1 mm Hg (mean +/- s.e. mean), P less than 0.001), stroke volume (4.9 +/- 0.8 ml m-2, P less than 0.05), total peripheral resistance (243 +/- 27 dyn s cm-5 m2, P less than 0.001) and forearm vascular resistance (1.3 +/- 0.3 mm Hg ml-1 min, P less than 0.01) and reduced the ratio of pre-ejection period to ventricular ejection time (-0.031 +/- 0.003, P less than 0.05) and forearm blood flow (-2.6 +/- 0.5 ml min-1, P less than 0.05) but did not affect heart rate or cardiac index. 3. Two Boots Cold Relief tablets (containing phenylephrine 10 mg and caffeine 60 mg) caused a small and short-lived increase in total peripheral resistance but did not have consistent effects on other measurements. Two Boots Pain Relief tablets (containing caffeine 60 mg) did not have important cardiovascular effects. 4. The cardiovascular effects of phenylpropanolamine, including vasoconstriction and an increase in cardiac performance, are consistent with its alpha- and beta 1-adrenoceptor agonist action. While it may help the symptoms of rhinitis, its use in patients with heart disease or hypertension is hazardous.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:A comparison of the cardiovascular effects of phenylpropanolamine and phenylephrine containing proprietary cold remedies. 172 92

The aim of this study was to investigate whether caffeine stimulates selectively renal vein renin levels at the side of unilateral stenosis in patients with renovascular hypertension. In this study seven of the involved patients had renal arterial stenosis and four had no stenosis. Four of the seven patients with a stenosis had retrospectively-proven renovascular hypertension. Renal vein renin sampling was performed before and after intravenous administration of caffeine. Caffeine did not induce any consistent effect on plasma renin activity in the renal veins, either on the stenotic side or on the contralateral side in patients with renovascular hypertension. There were no consistent caffeine mediated changes in systemic plasma renin activity.
 ...
PMID:The effect of caffeine on renal vein renin concentration in patients with renal arterial disease. 152 71

We investigated possible relations between excitation-contraction coupling and atrial natriuretic factor (ANF) release in rat atrial muscle using the isolated perifused atria preparation. To this purpose, the extracellular ionic environment was manipulated by replacement of Ca2+ with the polyvalent cations Ba2+, Sr2+, and La3+. Intracellular Ca2+ was altered by treatment with caffeine and ryanodine and by chemical (49 mM K+) depolarization. Replacement of Ca2+ with Ba2+ or Sr2+ abolished atrial spontaneous mechanical activity but did not prevent ANF release. Chemical depolarization also abolished spontaneous mechanical activity and significantly reduced ANF release in Ca(2+)-free media and in 0.625 mM extracellular Ca2+ but had no effect in the presence of 1.25 or 2.5 mM Ca2+, suggesting that changes in cytosolic Ca2+ levels do not affect ANF release in media containing Ca2+ in the physiological concentration range. The kinetics of ANF release observed during caffeine (10(-6) to 10(-2) M) treatment was similar to that seen in atrial preparations without treatment. At 10(-2) M, caffeine induced an increase in atrial beating rate and resting tension. Ryanodine (10(-4) M) pretreatment reduced stretch-induced ANF release by an average 34%, in addition to inhibiting tension development and beating. These findings clearly show marked differences between atrial cardiocytes and most other endocrine cells in terms of the effect of specific changes in the ionic environment on the secretory response; they also support the view that basal ANF release from atrial cardiocytes is not dependent on contractile atrial activity or Ca2+. In fact, Ca2+ appears to tonically inhibit the rate of basal ANF release. We conclude that, although indispensable for excitation-contraction coupling, intracellular Ca2+ transients by influx or from intracellular stores are not essential for basal ANF release. However, a ryanodine-sensitive compartment appears to be partly responsible for the increased ANF output after muscle stretch.
Hypertension 1991 Nov
PMID:Stretch-secretion coupling in atrial cardiocytes. Dissociation between atrial natriuretic factor release and mechanical activity. 183 55

One common nutrient postulated to be protective against osteoporosis, hypertension, and colon cancer is dietary calcium. We report here nutrient patterns by calcium intake in older adult residents of a geographically defined community in Southern California. The analysis included all 426 men and 531 women aged 50-79 y with complete 24-h diet data. Nutrient-density-adjusted calcium intake was divided into tertiles: low intake (less than 284 mg/1000 kcal), mid intake (284-440 mg/1000 kcal), and high intake (greater than 440 mg/1000 kcal). The distribution of the reported 24-h nutrient density of protein, fat, fiber, caffeine, trace minerals, vitamin D, and vitamin C was examined in relation to the calcium-intake tertiles. In both men and women, the adjusted intakes of protein, saturated fatty acids, vitamin D, magnesium, and phosphorus were significantly higher in the high-calcium-intake group than in the low- and mid-calcium-intake groups. In both men and women, alcohol intake was significantly lower in the high-calcium-intake group. Studies postulating a protective role for calcium will need to consider the multicolinearity in the Western diet.
 ...
PMID:Calcium intake: covariates and confounders. 184 36

We measured plasma concentrations of immunoreactive endothelin-1 (irET-1) in the prehypertensive and hypertensive phases in spontaneously hypertensive rats (SHR) and in malignant hypertension caused by deoxycorticosterone acetate (DOCA)-salt administration in SHR. We also measured concentrations of this peptide in another model of malignant hypertension, the two-kidney, one clip (2K1C) renovascular hypertensive rats chronically given caffeine. Plasma irET-1 concentrations in young (6-week-old) and mature (18-week-old) SHR did not differ from those of age-matched Wistar-Kyoto (WKY) rats. Four weeks of treatment with DOCA-salt increased blood pressure, blood urea nitrogen, serum creatinine, and plasma irET-1 in SHR but not in WKY rats. Eight weeks of DOCA-salt treatment further increased these values in SHR. Plasma irET-1 concentrations were not increased in the 2K1C rats. Six weeks of caffeine administration increased blood pressure, blood urea nitrogen, serum creatinine, plasma renin activity, and plasma irET-1 in the 2K1C rats but not in the sham-operated rats. High-performance liquid chromatographic profiles of plasma extracts pooled from these rats with malignant hypertension showed that a major component of irET-1 eluted in the position of synthetic ET-1 (1-21). Furthermore, acute hypertension induced by angiotensin II or phenylephrine did not affect the plasma irET-1 concentration in rats. The results suggested that the plasma ET-1 concentration is increased in rat models of malignant hypertension and that the high blood pressure itself is not the main factor involved in the increase of plasma ET-1.
Hypertension 1991 Jul
PMID:Plasma immunoreactive endothelin-1 in experimental malignant hypertension. 186 Jul 18


1 2 3 4 5 6 7 8 9 10 Next >>