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[Interrelations between blood pressure, blood volume, plasma renin and urinary catecholamines during beta-blockade in essential hypertension (author's transl)].

Studies in 55 patients with benign essential hypertension showed that the beta-blockers bufuralol (22 patients) and propranolol (33 patients) at a dose ratio of 1:4, possess comparable antihypertensive efficacy despite different properties regarding intrinsic sympathomimetic activity. Beta-blocker-monotherapy normalized blood pressure ( less than 140/90 mm Hg) in one fourth of the patients. Body weight and plasma and blood volumes remained unchanged during beta-blockade of four to six weeks duration, the mean plasma potassium was slightly increased. The inhibition of plasma renin activity (PRA) was more pronounced with propranolol (-69%) than with bufuralol (-47%). Wirth both beta-blockers decreases in blood pressure correlated inversely with pre-treatment PRA (p less than 0.05). Propranolol-induced changes in blood pressure correlated also with associated changes in PRA (p less than 0.005); in contrast, no such relationship was observed with bufuralol. The blood pressure effects of bufuralol, however, correlated significantly with changes in urinary noradrenaline excretion (r=0.41; p less than 0.05). Patient sub-groups with low, normal or high pre-treatment PRA in the average showed a comparable pattern of pre-treatment noradrenaline excretion and patients with normal renin levels exreted more adrenaline than those with low renin levels (p less than 0.001). These data are consistent with the concept that in untreated essential hypertension PRA may be an index of adrenergic activiity, the latter representing an important determinant of blood pressure response to beta-blockade. The blood pressure lowering effects of bufuralol in benign essential hypertension seem to be independent of renin and may be related, at least partly, to diminished free peripheral noradrenaline levels.

Adrenergic beta-Antagonists

Cadmium effects in rats on tissue iron, selenium, and blood pressure; blood and hair cadmium in some oregon residents.

Exposure of rats to cadmium causes a marked depletion of iron in liver and kidney. Selenium neither counteracts or intensifies the influence of cadmium on tissue iron levels. Selenium injections protect against cadmium-induced testicular damage but cause this element to accumulate in the testes at higher concentration than in animals exposed to cadmium without selenium. Selenium injection diverts the binding of cadmium from low molecular weight proteins to high molecular weight ones. Dosing rats with selenium and cadmium or inclusion of Se or Cd in the diet did not result in altered cadmium binding in tissues, raising some questions concerning the environmental significance of these injection experiments. Addition of selenium to a diet containing cadmium decreased the accumulation of cadmium in liver and kidney, but increased its deposition in testes. The metabolism of cadmium bound to metallothionein was markedly different as compared to the inorganic salt of this element. Dietary ascorbate, but not citrate or cysteine, decreased the deposition of cadmium in rat tissues. In some low-level exposure experiments with cadmium (1 to 1000 ppb), no differences were found in the percentage of dose absorbed or rate of cadmium accumulation when provided in food versus water. Female rats tended to absorb more cadmium than males. The binding of cadmium to cytosolic proteins was found to be different between rats fed low levels of cadmium (up to 1 ppm) as compared to those fed high levels of this element (100 ppm). Cadmium was not found to contribute to hypertension in rats, and a summary of results by various investigators is presented. Blood and hair cadmium levels in Oregon residents were found to be highest in employees of a mine, and hair cadmium was found to be respectively higher in smokers than nonsmokers and in metal workers than office workers. No relationships were observed in humans between blood or hair cadmium levels and blood pressure.

Animals

Chronobiology of blood pressure.

Blood pressure in normal and hypertensive subjects shows circadian variability with the minima during the hours of sleep. The factors influencing blood pressure show circadian variability, in particular, plasma and urinary aldosterone, plasma deoxycorticosterone and urinary sodium (factors implicated in cardiac output), angiotensin II as measured by plasma renin activity, plasma and urinary epinephrine and norepinephrine, and plasma and urinary prostaglandins of the E series (factors implicated in peripheral resistance). Direct causal relationships have not been established. The treatment of hypertensive subjects in relation to the circadian variability is reviewed.

Aldosterone

Organ blood flow, cardiac output, arterial blood pressure, and vascular resistance in rats exposed to various oxygen pressures.

Blood flow in different organs, cardiac output, and arterial blood pressure were measured in unanesthetized rats under 1, 2, 3.5, 5, and 7 ATA O2, during first electrical discharge developed at 7 ATA O2 and following decompression. Brain, spinal cord, and hypophysis blood flow were reduced after 10 min of exposure to 2, 3.5, and 5 ATA O2 and were normal before and during first electrical discharge. Liver and muscle blood flow were significantly reduced under all investigated pressures, while myocardium, lung, kidney, and adrenal blood flow remained unchanged except for a significant increase in myocardium and lung blood flow under 1 ATA O2. Cardiac output was significantly decreased while arterial blood pressure was significantly decreased under all investigated pressures. The total peripheral resistance increased 36 to 81% at various oxygen pressures. These results are discussed in relation to the possible involvement of hemodynamic changes in awake animals, in the development of the adverse effects of HOP.

Adrenal Glands

[The influence of vasodilatators on intraocular pressure and blood pressure (author's transl)].

The influence of different vasodilatators on blood pressure and intraocular pressure has been tested in animal experiments. For that purpose substances with alphasympathicolytic effect (Hydergin, Trental) have been tested as well as substances which are of direct influence on the muscles. In all cases a decrease of the blood pressure was noticed. Furthermore in most of the cases an increase of the intraocular pressure could be seen. This is due to a direct dilatation of ocular vessels. The effects were short-lived and reversible. We tried to find an explanation for the variations of intraocular pressure during the decrease of blood pressure. The low transmural pressure (PTM) and the corresponding low starting point of the muscle tonus seemed to be responsible for this phenomenon. Without doubt the starting point of the blood pressure, the dose, and the cardiac ability for compensation are of great influence in the development of the curve. Only a sufficiently high blood pressure is able to dilate the ocular vessels, so that one has to draw therapeutic conclusions from the constellation blood pressure/intraocular pressure before deciding on treatment.

Animals

Age, adiposity, blood pressure and blood lipids in a rural New Zealand population.

Multiple regression analysis of data on age, blood pressure, adiposity and blood lipids from a rural New Zealand population of over 1200 adults has been undertaken. The results show that rises in blood lipids over time in the population are independent of age and correlate significantly with adiposity. Thus plasma cholesterol and triglycerides correlate with adiposity (expressed as Quetelet's index or skinfold thickness) in men whereas significant correlation in women was only between adiposity and plasma triglycerides. Systolic and diastolic blood pressure in men was strongly correlated with their plasma triglycerides, but not cholesterol, when the effect of age and adiposity was removed. In women however only a weak correlation was observed between plasma triglycerides and systolic blood pressure. The significance of the findings is discussed.

Adult

Reduced nicotinamide adenine dinucleotide fluorescence and cortical blood flow in ischemic and nonischemic squirrel monkey cortex. 2. effects of alterations in arterial carbon dioxide tension, blood pressure, and blood volume.

The fluorescence of reduced nicotinamide adenine dinucleotide (NADH) from cerebral cortex was measured before, during, and after middle cerebral artery (MCA) occlusion and then at death of the animal. In normal cortex, NADH remained constant throughout a wide range of variations in blood pressure and Paco2. In ischemic cortex, NADH levels were higher in hypovolemic hypotensive animals than in normotensive normovolemic animals. Neither hypercapnia nor hypocapnia was effective in decreasing NADH in regions of ischemia, but the latter was associated with a degree of hypotension that interfered with interpretation of data. NADH returned to normal with restoration of flow, supporting the reversibility of this degree of ischemia. The high levels of NADH at death, compared to those during ischemia, are consistent with incomplete ischemia in this model of cerebral infarction.

Animals

Effects of decreasing arterial blood pressure on cerebral blood flow in the baboon. Influence of the sympathetic nervous system.

The influence of the sympathetic nervous system on the cerebral circulatory response to graded reductions in mean arterial blood pressure was studied in anesthetized baboons. Cerebral blood flow was measured by the 133Xe clearance method, and arterial blood pressure was decreased by controlled hemorrhage. In normal baboons, the constancy of cerebral blood flow was maintained until mean arterial blood pressure was approximately 65% of the base-line value; thereafter, cerebral blood flow decreased when arterial blood pressure was reduced. Superior cervical sympathectomy of 2-3 weeks duration did not affect the normal response. In contrast, both acute surgical sympathectomy (cervical trunk division) and alpha-receptor blockade (1.5 mg/kg of phenoxybenzamine) enhanced the maintenance of cerebral blood flow in the face of hemorrhagic hypotension in that cerebral blood flow did not decrease until mean arterial blood pressure was approximately 35% of the base-line value. The results indicate that the sympathetic nervous system is not involved in the maintenance of cerebral blood flow in the face of a fall in arterial blood pressure. Indeed, the implication is that the sympathicoadrenal discharge accompanying hemorrhagic hypotension is detrimental to, rather than responsible for, cerebral autoregulation.

Adrenergic alpha-Antagonists

[The influence of changes in body position on intraocular pressure, episcleral venous pressure, and blood pressure (author's transl)].

The intraocular pressure, the ophthalmic artery pressure, and the episcleral venous pressure increased after changes from sitting to recumbent body position, whereas the subclavian artery pressure remained unchanged or decreased slightly. Changing from recumbent to sitting position was followed by a decrease in IOP, ophthalmic pressure, and subclavian artery pressure. Comparing the last measurement in the first position to the first value after change, it was found that the IOP alters by about 20%, the ophthalmic artery pressure by 15%, and the episcleral venous pressure by 50%. In all series a decrease in subclavian artery pressure was observed during the first 15 min. The mean pressure in the ophthalmic artery diminished in the series that changed from sitting to recumbent position, whereas it increased in the other series during the first 15 min. The episcleral venous pressure increased more than the corresponding IOP after changing to the recumbent position.

Blood Pressure

The effect of cyclical administration of levonorgestrel and ethinyloestradiol on blood pressure, body mass, blood glucose and serum triglycerides.

The effects of two differing dosage schedules of ethinyloestradiol and levonorgestrel, taken cyclically as oral contraceptives, on blood pressure, body mass, blood glucose and serum triglycerides were measured. After 12 months there were no significant changes in systolic and diastolic blood pressure or blood glucose levels. There was a small but statistically significant increase in body mass after 1 year in the group taking levonorgestrel 15 microgram and ethinyloestradiol 30 microgram (P < 0,02), but not in the other group, although the mass in this group was significantly increased after 3 months of therapy. There was a statistically significant increase in serum triglycerides in the group taking levonorgestrel 50 microgram with ethinyloestradiol 50 microgram for 11 days, followed by levonorgestrel 125 microgram for 11 days, followed by levonorgestrel 125 microgram with ethinyloestradiol 50 microgram for 10 days. This effect appears to be dose-related and progressive with continued therapy; the significance of these results is discussed.

Adolescent

Reassessment of the effect of oral l-arginine on blood pressure: A systematic review and meta-analysis based on ambulatory blood pressure monitoring.

OBJECTIVE: This meta-analysis aimed to evaluate the effect of oral l-arginine supplementation on ambulatory blood pressure (ABP). METHODS: A systematic search of PubMed, Cochrane Library, Embase, and Web of Science databases was conducted from their inception through March 1, 2026. Randomized controlled trials (RCTs) assessing the effects of oral l-arginine intervention were included. Outcome measures included 24-h systolic blood pressure (24h SBP), 24-h diastolic blood pressure (24h DBP), daytime systolic blood pressure (dSBP), daytime diastolic blood pressure (dDBP), nighttime systolic blood pressure (nSBP), and nighttime diastolic blood pressure (nDBP). Meta-analysis was performed using Stata 17.0. The weighted mean difference (WMD) was used as the effect size, and the results were pooled with 95% confidence intervals (CIs). RESULTS: A total of 5 RCTs comprising 202 participants were included. Meta-analysis results demonstrated that oral l-arginine significantly reduced 24h SBP (WMD&#x202f;=&#x202f;-4.23&#x202f;mmHg, 95% CI [-5.87, -2.58]; P&#x202f;<&#x202f;0.01) and 24h DBP (WMD&#x202f;=&#x202f;-3.04&#x202f;mmHg, 95% CI [-4.48, -1.59]; P&#x202f;<&#x202f;0.01). Significant reductions were also observed for dSBP (WMD&#x202f;=&#x202f;-4.16&#x202f;mmHg, 95% CI [-5.90, -2.41]; P&#x202f;<&#x202f;0.01) and dDBP (WMD&#x202f;=&#x202f;-4.25&#x202f;mmHg, 95% CI [-5.85, -2.66]; P&#x202f;<&#x202f;0.01). Furthermore, oral l-arginine significantly lowered nSBP (WMD&#x202f;=&#x202f;-5.70&#x202f;mmHg, 95% CI [-7.81, -3.58]; P&#x202f;<&#x202f;0.01) and nDBP (WMD&#x202f;=&#x202f;-4.18&#x202f;mmHg, 95% CI [-6.27, -2.09]; P&#x202f;<&#x202f;0.01). CONCLUSION: Oral l-arginine supplementation significantly reduces ABP. However, the number of included studies was limited, and further validation through additional relevant research is warranted.

Arginine