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PubMed1987

Diltiazem maintains renal vasodilation without hyperfiltration in hypertension: studies in essential hypertension man and the spontaneously hypertensive rat.

The systemic and renal hemodynamic effects of diltiazem were determined in patients with mild to moderately severe essential hypertension and in rats with spontaneous hypertension (SHR). Seven patients were treated for one full year (300 mg/day, average dose) and 10 SHR and 10 normotensive Wistar-Kyoto (WKY) rats received 1 and 2 mg/kg, intravenously. In both man and rat with genetic hypertension, arterial pressure was reduced through a fall in total peripheral resistance without associated reflexive increases in heart rate and cardiac index; and the patients demonstrated no change in plasma volume. In both man and the SHR: renal blood flow increased (in SHR not statistically significant) as arterial pressure and renal vascular resistance fell; glomerular filtration rate (GFR) remained unchanged and the filtration fraction (FF) significantly fell; and calculated intrarenal hemodynamic indices (using the Gomez formulae) demonstrated falls in afferent and efferent glomerular arteriolar pressures and resistances and in intraglomerular pressures, thereby explaining the unchanged GFRs and the decline in FF. These findings in both hypertensive man and rat are in contrast with those of the normotensive WKY that only demonstrated a fall in afferent glomerular arteriolar resistance. Thus, these data demonstrate that diltiazem controlled arterial pressure in both forms of genetic hypertension associated with falls in systemic and renal arteriolar resistances and with improved intrarenal hemodynamics without glomerular hyperfiltration.

Adult↗
PubMed1988

[Intracellular free calcium and plasma calcium in patients with essential hypertension. Is there a correlation between extracellular and intracellular disorders of calcium regulation in essential hypertension?].

Alterations in intracellular free calcium regulation as well as disturbances of extracellular calcium homeostasis have been observed in patients with essential hypertension. It has been hypothesized that a generalized defect of calcium regulation might be of importance in the pathogenesis of essential hypertension. In one hypothesis a primary calcium-deficiency in essential hypertension has been linked to subsequent membrane instability and altered intracellular free calcium concentrations. We therefore investigated the relationship between intracellular free calcium concentrations in platelets and ionized as well as total plasma calcium in patients (n = 38) with essential hypertension and in age-matched normotensive subjects (n = 35). Intracellular free calcium in hypertensive patients was elevated by 13% (p less than 0.05) although there was a wide overlap between the values of the two groups. However, no difference with regard to the ionized or total plasma calcium concentrations could be observed. Total plasma calcium concentration, ionized plasma levels as well as intracellular free calcium were positively correlated (p less than 0.05) with mean arterial blood pressure. No correlation however was found between the extracellular and intracellular calcium compartments. We therefore could not observe a generalized defect of calcium regulation in essential hypertension, and extracellular calcium concentrations do not seem to be related to intracellular calcium derangement in this disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Glucocorticoid sensitivity of circulating monocytes in essential hypertension.

BACKGROUND: Essential hypertension ranks among the strongest cardiovascular risk factors. Cytokine production by monocytes plays a key role in atherosclerosis development and acute coronary syndromes. We investigated whether stimulated monocyte cytokine release and its inhibition by glucocorticoids would differ between hypertensive and normotensive subjects. METHODS: Study participants were 222 middle-aged male employees with industrial jobs. Following the criteria of the World Health Organization/International Society for Hypertension, 76 subjects were classified as being hypertensive (systolic blood pressure > or = 140 mm Hg or diastolic blood pressure > or = 90 mm Hg). In vitro monocyte tumor necrosis factor (TNF)-alpha release after lipopolysaccharide (LPS) stimulation was assessed with and without coincubation with incremental doses of dexamethasone. Monocyte glucocorticoid sensitivity was defined as the dexamethasone concentration inhibiting TNF-alpha release by 50%. RESULTS: Hypertensive subjects showed 11% higher LPS-stimulated TNF-alpha release than normotensive subjects (F(1,181)= 5.21, P =.024). In hypertensive subjects, monocyte glucocorticoid sensitivity was 21% lower than in normotensive subjects (F(1,178)= 4.94, P =.027), indicating that dexamethasone inhibited relatively less TNF-alpha release in hypertensive subjects. Results held significance when a set of classic cardiovascular risk factors was controlled for. CONCLUSION: The findings suggest that proinflammatory activity of circulating monocytes is higher in hypertensive than in normotensive men, providing one potential pathway to explain the increased atherosclerotic risk with essential hypertension.

Adult↗
PubMed2006

Angiotensinogen promoter sequence variants in essential hypertension.

BACKGROUND: Essential hypertension is a complex multifactorial disease caused by ill-defined genetic factors. The angiotensinogen (AGT) gene has been implicated as a risk factor in essential hypertension. METHODS: To assess the role of AGT in hypertension, we evaluated two polymorphisms (A-6G and C-20A) in the 5' region of the gene that have been shown to have a role in transcriptional regulation. A total of 463 subjects were studied: 243 African Americans (26 male and 34 female normotensives, 66 male and 117 female hypertensives) and 220 whites (35 male and 60 female normotensives, 55 male and 70 female hypertensives). African American and white subjects were examined individually, as significant differences in allele and genotype frequencies were observed between these two cohorts. RESULTS: White female hypertensives and normotensives differed significantly in genotype frequency at C-20A (P = .02). No other single site comparisons were significantly different between hypertensives and normotensives in either the white or African American samples. Haplotype frequencies in white males also differed significantly between phenotypic classes (P = .05). To evaluate the data further, we assessed all polymorphic sites simultaneously by the examination of multisite interaction and determined the single best genetic model for each population. A model that included both sites and gender correctly predicted hypertension status in the white population 59.1% of the time (P = .039). The model generated for the African American population was not significant. CONCLUSIONS: Our results suggest that a complex set of genetic factors interact with gender to predispose whites to hypertension.

Adenine↗
PubMed1996

Modifications induced by -10 degrees Trendelenburg's posture in sodium tubular handling in patients with essential hypertension.

In essential hypertensive patients "exaggerated natriuresis" is a response to acute volume expansion. However, the underlying mechanisms for this remain to be determined. We studied 19 patients with essential hypertension (HP) and 9 normotensive subjects (NS). In all examined subjects the response to acute central volume expansion, without the plasma compositional change that Trendelenburg's position involves, was evaluated during 90 min (period T) after a similar period of deambulation (period D). Mean blood pressure (MBP), tubular sodium handling by the lithium clearance technique, plasma renin activity (PRA), plasma aldosterone (PA), plasma catecholamines and urine prostaglandine E2 and kallikrein were assessed after D and T. MBP was significantly higher in HP than in NS (p = 0.00001). HP showed "exaggerated natriuresis" after T (fractional excretion of sodium increased from 0.55 +/- 0.1% after D to 1.20 +/- 0.2% after T, p < 0.01). This was because of a decrease in their proximal fractional reabsorption of sodium (from 74.96 +/- 1.8% after D to 62.50 +/- 2.8% after T, p < 0.01). Plasma epinephrine and plasma dopamine after T were significantly lower than in standing position in HP (p < 0.01) but no in NS. The decrease in plasma renin activity after T in HP was 53%, and 32% in NS. There were not any significant differences between groups in the other neurohormonal systems studied. We conclude that the major determinant of "exaggerated natriuresis" in hypertensive patients is a higher stimulation of the cardiopulmonary receptors following Trendelenburg's position and consequently stronger reflex inhibition of sympathetic system activity and renin-angiotensin II activity. The "exaggerated natriuresis" after Trendelenburg's position in HP was an expression of abnormal pressure natriuresis.

Adult↗
PubMed1999

Quantitative association between a newly identified molecular variant in the endothelin-2 gene and human essential hypertension.

BACKGROUND: Essential hypertension is a multifactorial disease in which the genetic contribution is probably the result of a number of genes acting in combination. Recent work has incriminated endothelin-2 (ET2) as a candidate gene for human essential hypertension. This study sought to (i) determine the existence of any molecular variants in the ET2 gene; (ii) undertake an allelic-association study of any such variants found in a large group of well characterized hypertensive and control populations; and (iii) assess any quantitative relationship between the molecular variant and pretreatment blood presure. METHODS: The ET2 gene was subjected to single strand conformation polymorphism (SSCP) analysis in order to identify novel molecular variants. Well-characterized subjects recruited from our local population were used in our association study. Two hundred and forty-four hypertensive patients with pre-treatment blood pressure (range 139/94-237/133 mmHg) were well matched with 228 controls from our local population of 30000 healthy subjects (range 96/62-160/85 mmHg). All subjects were Caucasian. RESULTS: Polymerase chain reaction-SSCP identified a single A985G base change in 3'-UTR of the ET2 gene which was confirmed by direct sequencing. A restriction site for the enzyme BsmA1 was either created (+) or removed (-) with this polymorphism. Analysis of variance showed that the ET2 genotype was an independent predictor of pre-treatment diastolic blood pressure (DBP) in the hypertensive (P< 0.001) but not normotensive group with higher pressures tracking with the (-) allele. Other covariates such as age, sex, alcohol, cigarette smoking, body mass index and cholesterol showed no significant relationship with this genotype. The genotype frequencies for the hypertensive and control population were (-/-: -/+: +/+) 178 :58:8 and 168:55: 5, respectively (not significant). Subjects from the top and tail quartiles of measurement of blood pressure in both groups were selected for genotype and allele frequency comparison. Both genotype and allele differences were highly significant between the two extreme groups for DBP (genotype P< 0.001, alleles P< 0.01) distribution. A search for potential functional variants in linkage disequilibrium with A985G found one further variant in the 5'-UTR, C44T. Conditional haplotype probabilities in 214 chromosomes show that this polymorphism is not in linkage disequilibrium with the 3'-UTR. No other variants were found on a molecular screen of the transcribed portion of the ET2 gene. CONCLUSION: This newly identified polymorphism of the ET2 gene tracked significantly in hypertensives when blood pressure was assessed as a quantitative trait. The difference in genotype and allele frequencies between the extremes of blood pressure suggest that the ET2 locus influences the severity rather than the initial development of hypertension.

3' Untranslated Regions↗
PubMed1990

Systemic and renal effects of a new angiotensin converting enzyme inhibitor, benazepril, in essential hypertension.

Seventeen essential hypertensive patients with normal renal function were treated with a new non-sulphydryl orally active angiotensin converting enzyme (ACE) inhibitor, benazepril, 10 mg given once or twice daily, according to diastolic blood pressure levels, for 6 weeks. In all patients, changes in blood pressure, systemic and renal hemodynamics, plasma renin activity and urinary aldosterone and albumin excretions were assessed at the end of a 2-week placebo run-in period and at the end of the study. Benazepril monotherapy controlled blood pressure well. No changes in cardiac output, heart rate or stroke volume were observed, while peripheral vascular resistance was significantly decreased (-11%, P less than 0.05). Plasma volume was unaltered. The glomerular filtration rate was stable, but effective renal plasma flow was increased because of the marked reduction in renal vascular resistance (-35%) and, therefore, the filtration fraction was decreased. Urinary albumin excretion remained unchanged. A significant increase in plasma renin activity (P less than 0.001) and a decrease in urinary aldosterone excretion were seen. No side effects were observed during the treatment period. In conclusion, our results suggest that benazepril alone is an effective antihypertensive agent in patients with essential hypertension. The blood pressure lowering effect is due mainly to systemic vasodilation and is observed up to 24 h after administration of the drug. The vasodilation appears to be more consistent in the renal than in the systemic circulation.

Adult↗
PubMed1992

Sib pair linkage analysis of renin gene haplotypes in human essential hypertension.

Although essential arterial hypertension is believed to have a strong genetic predisposition, the gene(s) responsible are unknown. The mechanisms underlying the regulation of blood pressure and experimental studies place the renin gene among the main candidate genes that need to be tested in humans. We tested the hypothesis of a linkage between the renin gene and essential hypertension using the affected sib pair method. Siblings (133 subjects, 52.1 +/- 10.9 years) from 57 families were selected for sustained hypertension (160.7 +/- 22.9/99.5 +/- 12.8 mmHg with 80% of patients under antihypertensive treatment), of early onset (40.7 +/- 12.0 years), in the absence of obesity, diabetes mellitus, and secondary hypertension. Eight renin haplotypes were generated from three diallelic renin restriction fragment length polymorphisms (RFLPs) (TaqI, HinfI, HindIII) located throughout the renin gene. The allelic concordance between the sib pairs was analyzed by identity by state relationships for 98 sib pairs (41 for 41 couples, 39 for 13 trios, 18 for 3 quartets). Allelic frequencies in the 57 hypertensive probands were similar to those observed among 102 hypertensive subjects studied previously. Six of eight possible haplotypes were observed, the informativity of the marker corresponded to 70% of heterozygosity. Allelic concordance for all sib pairs according to sibship size was not significantly different from that expected under the hypothesis of no linkage (t = 0.52, P = 0.15) reflecting only a small excess of renin alleles shared by the hypertensive sibs (1.44 +/- 0.6 vs 1.36 +/- 0.6). Likewise the linkage hypothesis was unsupported by weighted estimates to correct for possible bias due to large sibship size. Thus, the sib pair analysis suggests that the renin gene does not have a frequent role in the pathogenesis of essential hypertension; further more powerful linkage studies or other approaches will be needed to detect contributions at the renin locus to the heritability of essential hypertension.

Alleles↗
PubMed2000

[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?].

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).

Acetylglucosaminidase↗
PubMed1998

Expression of altered alpha2-adrenergic phenotypic traits in normotensive humans at genetic risk of hereditary (essential) hypertension.

BACKGROUND: Essential (hereditary) hypertension is a common, though complex, trait with substantial heritability, but a still-obscure mode of inheritance. In this disorder with relatively late onset, knowledge of phenotypes with earlier penetrance would aid genetic analyses, as well as assessment of risk. OBJECTIVE: Because alpha2-adrenergic receptor alterations are among the most heritable in experimental genetic hypertension, we hypothesized enhanced expression of alpha2-adrenergic phenotypic traits in still-normotensive humans at genetic risk of hypertension. METHODS: We evaluated hemodynamic (blood pressure, cardiac output, systemic vascular resistance, stroke volume, and cardiac contractility) and biochemical (plasma drug, catecholamine, renin, and chromogranin A levels) responses to alpha2-adrenergic blockade with intravenous yohimbine in 84 normotensive subjects stratified by genetic risk of essential hypertension (67 with positive family histories and 17 with negative family histories of hypertension), as well as 18 subjects with established essential hypertension. Results were evaluated by analysis of variance, normal likelihood ratio test, and by maximum likelihood analysis for bimodality (i.e. mixtures) of response distributions. RESULTS: Blood pressure rose (P<0.001) during alpha2-adrenergic blockade, with greater response (P<0.001) in members of the hypertensive than in members of the normotensive group. Hemodynamically, the rise in blood pressure resulted from an increase in cardiac output (P<0.001), with associated increases in stroke volume (P=0.002) and cardiac contractility (P=0.006), without an overall change in systemic vascular resistance. Biochemically, plasma norepinephrine (P<0.001), epinephrine (P=0.001), and chromogranin A (P=0.02) rose, suggesting augmentation of efferent exocytotic sympathoadrenal activity. Cardiac output and stroke volume responses were correlated to increments in plasma catecholamines (especially epinephrine) for the positive group, but not for the negative group. Baseline plasma catecholamines predicted increments of stroke volume after administration of yohimbine (P=0.003-0.007) for the positive but not for the negative group. Simultaneous comparison of means and variances of cardiac output and stroke volume alpha2-adrenergic responses, by using a normal likelihood ratio test, revealed highly significant (P=0.025 to P<0.0001) differences between the groups of subjects with and without family histories of hypertension. Frequency histogram suggested that there was a bimodal distribution of responses of stroke volume to alpha2-adrenergic blockade for the normotensive group with positive family histories of hypertension; maximum likelihood analysis strongly rejected the hypothesis of a unimodal distribution, whereas the hypothesis of bimodality could not be rejected (chi2=18.4, P=0.0004). The second (exaggerated) mode of response of stroke volume to alpha2-adrenergic blockade, defined by maximum likelihood analysis, was found for 9.5% of subjects in the normotensive group with positive family histories of hypertension, and was characterized by significantly different responses of cardiac output (P=0.001), stroke volume (P<0.001), contractility (P<0.001), heart rate (P=0.03), systemic vascular resistance (P<0.001), and epinephrine (P<0.001). Even prior to alpha2-adrenergic blockade, baseline stroke volume (P=0.01), heart rate (P=0.04), systemic vascular resistance (P=0.005), and catecholamine (P=0.001-0.005) values for this subgroup were different than control values. CONCLUSIONS: We conclude that heterogeneous, bimodally distributed hemodynamic responses to alpha2-adrenergic blockade in subjects with positive family histories of hypertension suggest a discrete subgroup with early expression of perhaps Mendelian traits associated with risk of later development of hypertension. Such phenotypic traits ('intermediate phenotypes'), with earlier penetrance than hypertension itself, can be

Adolescent↗
PubMed1995

[The significance of platelet alpha 2-adrenoceptor and sympathetic nerve activity in the hypertensive mechanism under essential hypertension--with special reference to pressor response to norepinephrine].

Although many studies have examined the metabolism of catecholamines and cardiovascular responsiveness to norepinephrine in essential and various experimental hypertension, the role of sympathetic nervous system in the pathogenesis of hypertension has not been elucidated. In this study, therefore,the role of sympathetic nerve activity related to platelet alpha 2-adrenoceptor was investigated to clarify the mechanism in which sympathetic nervous system augments the blood pressure elevation in patients with essential hypertension (EHT). Tritiated yohimbine binding was used to estimate platelet membrane alpha 2-adrenoceptor characteristics in 27 hospitalized patients with mild to moderate EHT and 27 normotensive subjects (NT) receiving a regular diet containing 120mEq/day of sodium and 75mEq/day of potassium. In this study, mean arterial pressure (MAP) and plasma norepinephrine concentration (pNE) was significantly higher in EHT than those in NT. Total binding sites (Bmax) and dissociation constant (Kd) for 3H-yoshimbine in EHT was also significantly higher than those in NT. There was a significant positive correlation between Bmax and age in NT, but not in EHT. A significant positive correlation was observed between the pressor response to infused norepinephrine (NE-R:increments in MAP induced by i.v. infused 0.2 micrograms/kg/min of NE) and Bmax both in NT and EHT. On the other hand, no significant correlation was found between NE-R and Kd in NT and EHT. In addition, Bmax was correlated inversely with PNE in both NT and EHT. These findings suggest that down-regulation mechanism exists in platelet alpha 2-adrenoceptor number responded to PNE levels. Moreover, the increased density of alpha-adrenoceptor might have something to do with the augmented NE-R in EHT, indicating an important pathophysiological role of this receptor in the hypertensive mechanisms in EHT.

Adult↗
PubMed1994

Effect of potassium on vasodilation to acetylcholine in essential hypertension.

Patients with essential hypertension show impaired endothelium-dependent vasodilation induced by acetylcholine. Because dietary potassium supplementation increases endothelium-dependent relaxations to acetylcholine in hypertensive rats, we designed the present study to investigate whether potassium increases endothelium-dependent vasodilation in essential hypertensive patients. Therefore, in patients with essential hypertension (n = 13) and in normotensive control subjects (n = 13) we evaluated the effect of intrabrachial potassium chloride (0.2 mmol/min) on forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 micrograms/100 mL forearm tissue per minute). In both groups of patients, potassium chloride infusion augmented local plasma potassium concentrations. Furthermore, in essential hypertensive patients but not in normotensive subjects it increased the vasodilating effect of the first three infusion rates of acetylcholine. In contrast, in seven adjunctive essential hypertensive patients, potassium chloride did not alter intrabrachial sodium nitroprusside-induced forearm vasodilation (1, 2, and 4 micrograms/100 mL forearm tissue per minute). Finally, to evaluate the role of nitric oxide on potassium-dependent facilitation of acetylcholine-induced vasodilation in essential hypertension, we studied the effect of intrabrachial NG-monomethyl L-arginine (100 micrograms/100 mL per minute) in another group of seven hypertensive patients. Vasodilation to acetylcholine was again increased by potassium chloride; NG-monomethyl L-arginine slightly blunted the vasorelaxing effect of acetylcholine but abolished the potentiating effect of potassium.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1997

High plasma endothelin-1 levels in hypertensive patients with low-renin essential hypertension.

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide derived from endothelial cells and may be important in the control of systemic blood pressure (BP) and local blood flow. Immunoreactive ET-1 plasma levels may be normal or elevated in human arterial hypertension, although the exact pathophysiological role of ET-1 remains to be established. The aim of our study was to determine the relationship between the components of the renin-angiotensin-aldosterone system and plasma ET-1 levels in patients with low, normal or high-renin essential hypertension. The study groups included 13 patients with low-renin essential hypertension (average age 43.5 +/- 16.2 years), 16 patients with normal-renin essential hypertension (46.5 +/- 13.4 years), 11 patients with high-renin essential hypertension (40.7 +/- 13.8 years) and 12 healthy subjects (43.1 +/- 11.4 years). Our results demonstrated that the mean ET-1 values of all patients with essential hypertension were 10.4 +/- 3.4 pg/ml; there was not a statistical correlation between plasma renin activity (PRA) and the ET-1 levels of hypertensives; instead there was a statistically significant correlation between plasma ET-1 and plasma aldosterone (PA) (r = 0.393; P < 0.026). In particular mean plasma ET-1 values in patients with low-renin essential hypertension (12.6 +/- 2.1 pg/ml) were significantly higher (ANOVA = 0.000, P < 0.05) than those of normotensive subjects (7.7 +/- 1.7 pg/ml), patients with normal-renin essential hypertension (8.5 +/- 2.8 pg/ml), and patients with high-renin essential hypertension (9.9 +/- 3.8 pg/ml), respectively. There was a statistical correlation between PA and ET-1 levels in patients with low-renin essential hypertension (r = 0.619, P < 0.024). Our study demonstrated that there was an increase of circulating ET-1 levels in patients with low-renin essential hypertension and ET-1 plasma levels correlated with PA. The results suggest that ET-1 may play an important role in this particular form of human essential hypertension.

Adult↗
PubMed1996

Defective L-arginine-nitric oxide pathway in offspring of essential hypertensive patients.

BACKGROUND: Essential hypertension is characterized by impaired endothelium-dependent vasodilation. The present study was designed to investigate whether this abnormality is a primary defect or a consequence of blood pressure increases. METHODS AND RESULTS: In offspring of essential hypertensive patients (n = 34) and normotensive subjects (n = 30), we evaluated forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 micrograms.100 mL-1.min-1), an endothelium-dependent vasodilator, and sodium nitroprusside (1, 2, and 4 micrograms.100 mL-1.min-1), an endothelium-independent vasodilator. Minimal forearm vascular resistances also were calculated as the ratio between mean intra-arterial pressure and maximal forearm blood flow induced by forearm ischemia and hand exercise. Vasodilation to acetylcholine was significantly (P < .01) blunted in offspring of hypertensive patients compared with offspring of normotensive subjects, whereas the responses to sodium nitroprusside and minimal forearm vascular resistances were similar. In two subgroups of 14 offspring of essential hypertensive patients but not in 10 offspring of normotensive subjects, vasodilation to acetylcholine was increased by intra-brachial L-arginine (1 mumol.100 mL-1.min-1), the substrate for nitric oxide synthesis, whereas in the other 10 and 8 offspring of essential hypertensive patients and normotensive subjects, respectively, cyclooxygenase blockade by intra-brachial indomethacin (50 micrograms.100 mL-1.min-1) was ineffective. CONCLUSIONS: Offspring of essential hypertensive patients are characterized by a reduced response to acetylcholine linked to a defect in the nitric oxide pathway, suggesting that an impairment in nitric oxide production precedes the onset of essential hypertension.

Acetylcholine↗
PubMed1979

Decrease of calcium binding by the red blood cell membrane in spontaneously hypertensive rats and in essential hypertension.

Ca binding in the red blood cell (RBC) membrane of spontaneously hypertensive rats (SHR) and of patients with essential hypertension was studied. Under conditions of physiological concentration of free Ca in the incubation medium of RBC the outer part of the membrane binds 393 +/- 32 and 435 +/- 30 nmole of Ca per ml of RBC in rats and humans, respectively, without essential differences in the amount of Ca in hypertensive individuals as compared to the normotensive controls. The membrane of red blood cell ghosts (RBCgh) at concentrations of free Ca corresponding to its intracellular concentration binds 4.28 +/- 0.39 and 3.53 +/- 0.15 nmole of Ca per mg of protein of RBCgh in rats and humans, respectively. This part of membrane-bound Ca pool (most probably related to the inner part of the red blood cell membrane) is reduced by 48% in SHR and by 28% in patients with essential hypertension as compared to normotensive controls. It is suggested that the decrease of Ca binding ability of the RBC membrane in both types of hypertension studied may be a pattern of a more widespread cell membrane defect.

Adolescent↗