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PubMed1989

Platelet cyclic AMP in essential hypertensive and normotensive offspring.

Essential hypertension is accompanied by several modifications to platelet metabolism suggesting hyper-reactivity to various aggregating agents. As the platelet response is mediated by both cytosolic free calcium, which is stimulatory, and cyclic (c)AMP, which is inhibitory, this hyper-reactivity may be caused by a modification in cAMP metabolism. We therefore determined cAMP in unstimulated platelets from 19 patients with essential hypertension and 27 age-matched normotensive subjects, nine with and 19 without a family history of hypertension. The platelet cAMP content was reduced in the essential hypertensives and in the normotensives with a positive family history by 37.5% and 42%, respectively (P less than 0.001 for both). Platelet cAMP was inversely correlated with diastolic blood pressure (P = 0.036). After prostaglandin (PG) E1 stimulation, the platelet cAMP content remained lower in the patients with essential hypertension than in the normotensive subjects, whatever their hypertensive heredity. The rises in cAMP caused by inhibition of phosphodiesterase by 7-bromo-1,5-dihydro-3,6-dimethylimidazo-[2,1-b]quinazolin-2[ 3H]-one (Ro 15-2041) were similar in the three groups. These results indicate that cAMP, the platelet inhibitory messenger, is reduced in hypertensive patients and in their normotensive offspring and may affect the various platelet abnormalities previously described in this disease.

Adult↗
PubMed1994

[Essential hypertension: psychosomatic aspects].

Essential hypertension is a heterogenous disease made up of several still unspecified subgroups. According to the dual theory of hypertension, acquired and genetic factors can lead to vascular muscle defects and increased sympathetic drive, which, either both or each alone, can lead to an increased vascular resistance. Acquired factors can either help a predisposition to become a manifest disease, act by itself to cause a disease or prevent a genetic trait from becoming manifest. Among the acquired factors, we differentiate those lying inside the personality, which means they are early acquired in life and those lying outside of the individual such as job-stress, noise exposure etc. How the external stressors are perceived depends upon the personality make up and the social support system. Within the presented model the Greek word 'crisis' plays an important role, since it characterizes a state in which a decision has to be made. In a situation in which a decision cannot be made in reality or tried out in fantasy life, the organism will activate the autonomic nervous system in a planless fashion, alternating very rapidly between its two branches, with concomitant symptoms of trembling, piloerection, salivation, vomiting, urination, defecation etc. In case this persists for a longer period of time the reciprocity between the two systems may break down, the organism seems to be psychologically immobilized. In the beginning of stress exposure, increased sympathetic nervous system activity is seen as an adaptive response, thereby enabling the individual to cope, but if the attempts to cope meet with constant failure, the stress becomes unbearable. The attitude of giving up which then develops is accompanied by a low level functioning of the sympathetic nervous system. This goes along with an adaptation for the baroreceptor depressor mechanism. As a consequence, any kind of additional stress would not lead to a relieving counterregulation. This might be a small stone within the mosaic of essential hypertension.

Adaptation, Psychological↗
PubMed1999

Vasodilation to bradykinin is mediated by an ouabain-sensitive pathway as a compensatory mechanism for impaired nitric oxide availability in essential hypertensive patients.

BACKGROUND: In essential hypertension, endothelium-dependent vasodilation is impaired because of reduced nitric oxide (NO) availability, which is mainly caused by oxidative stress. The present study was designed to identify the mechanism(s) responsible for NO-independent vasodilation to bradykinin in patients with essential hypertension. METHODS AND RESULTS: In 16 healthy subjects (49.5+/-5.8 years; 118.6+/-3.5/78.9+/-2.9 mm Hg) and 16 patients with essential hypertension (47.9+/-4.8 years; 154.6+/-4.5/102.9+/-3.2 mm Hg), we measured modifications in forearm blood flow (strain-gauge plethysmography) during intrabrachial infusion of bradykinin (5, 15, or 50 ng/100 mL of forearm tissue per minute) in the presence of saline, N(omega)-monomethyl-L-arginine (L-NMMA; used to inhibit NO synthase; 100 microg/100 mL of forearm tissue per minute), and ouabain (to block Na(+)K(+)/ATPase and prevent hyperpolarization; 0.7 microg/100 mL of forearm tissue per minute). In healthy subjects, vasodilatation to bradykinin was significantly blunted by L-NMMA and unaffected by ouabain. In hypertensive patients, vasodilatation to bradykinin was not modified by L-NMMA, but it was significantly reduced by ouabain. In an adjunctive group of 8 hypertensive patients (49.9+/-3.8 years; 155.9+/-5.5/103.7+/-3.9 mm Hg), the response to bradykinin was repeated during the administration of intrabrachial vitamin C (a scavenger for oxygen free radicals; 8 mg/100 mL of forearm tissue per minute). In these patients, L-NMMA-induced inhibition of vasodilation to bradykinin was restored, and ouabain was no longer effective. In a final group of 6 normotensive controls (45.9+/-4.1 years; 115.1+/-2.9/79.3+/-2.1 mm Hg), vasodilation to bradykinin residual to L-NMMA blockade was further inhibited by simultaneous ouabain infusion. CONCLUSIONS: Vasodilation to bradykinin is impaired in essential hypertensive patients because of an NO-system alteration caused by oxidative stress, and it is mediated by an alternative pathway, possibly involving endothelium-dependent hyperpolarization.

Adaptation, Physiological↗
PubMed1994

Insulin resistance--not hyperinsulinemia--is pathogenic in essential hypertension.

A correlation between essential hypertension and insulin resistance/hyperinsulinemia is well documented, and there is adequate reason to believe that this association is causal. The common presumption that hyperinsulinemia mediates this connection is based on studies demonstrating various pressor effects of insulin, such as sodium retention, activation of the sympathetic nervous system, and stimulation of renin output. However, a consideration of physiological parameters in essential hypertensives indicates that these insulin-mediated pressor effects are unlikely to play a crucial pathogenic role in most cases of essential hypertension. Moreover, physiological elevation of insulin following a meal is typically associated with a reduction of blood pressure in hypertensives and the elderly. Euglycemic insulin clamps tend to reduce blood pressure in elderly subjects, and prolonged maintenance of hyperinsulinemia in animals does not raise blood pressure. In fact, insulin has long been known to have direct vasodilatory or antipressor effects on resistance vessels, and there is recent evidence that insulin reduces vascular resistance in skeletal muscles to facilitate glycogen storage after a meal. I propose that essential hypertensives experience a net deficit of insulin activity in vascular muscle, and that, in conjunction with other genetic or acquired defects of electrolyte transport, this leads to an increase in basal vascular tone and a hypersensitivity to pressor agents. Correction of insulin resistance usually aids blood pressure control, and in addition may mitigate the excess cardiovascular risk associated with hypertension.

Animals↗
PubMed2006

Endothelial dysfunction and the kidney: emerging risk factors for renal insufficiency and cardiovascular outcomes in essential hypertension.

Renal insufficiency in essential hypertension represents the expression of a medium- and small-size arteriolopathy characterized by intimal hyperplasia, hyalinosis, and smooth muscle cell hypertrophy (nephroangiosclerosis). Because in animal models endothelial dysfunction plays a role in this alteration, nephroangiosclerosis and the attendant renal insufficiency may be the expression of a systemic dysfunction of vascular endothelium. Endothelial function in the kidney vasculature of hypertensive individuals has been investigated little because studies on the hemodynamic response of the kidney to nitric oxide activation and blockade are laborious to perform. There is no direct proof that endothelial dysfunction in the forearm or in the coronary circulation is paralleled by a similar hemodynamic dysfunction in the kidney. A recent study in a large population of patients with essential hypertension showed that, independent of other risk factors, the GFR in these patients is strongly related to the forearm blood flow response to acetyl choline (an established test of endothelial function). Furthermore, in this study, C-reactive protein was inversely related to the GFR and with the vasodilatory response to acetyl choline, pointing to inflammation as a likely mechanism to explain the association between endothelial dysfunction and impaired renal function in essential hypertension. A dysfunctional endothelium may represent a critical link accounting for the risk for both renal impairment and cardiovascular complications in essential hypertension.

Acetylcholine↗
PubMed1980

A Na+,K+ co-transport assay for essential hypertension.

In erythrocytes from essential hypertensive patients and some of their normotensive offspring, the Na+,K+ co-transport system is unable to transport Na+ in an uphill direction against the electrochemical Na+ gradient. Recent studies of the kinetic properties of this system have permitted us to further characterize the abnormal co-transport in hypertension. Thirty-four essential hypertensive patients were characterized by a two- to three-fold decrease in the maximal rate of the outward Na+,K+ co-transport and a partial uncoupling of this system as compared with 22 normotensive controls. On the other hand, a normal co-transport was found in five secondary hypertensives with no family history of hypertension, thus indicating that the abnormal co-transport is not the consequence of high blood pressure per se. An abnormal co-transport was also found in around 50% of 19 young normotensives born of one hypertensive parent, suggesting genetic transmission. This study allows us to propose the use of a specific Na+,K+ co-transport assay for the differential diagnosis between essential and secondary hypertension and for the detection of those normotensives born of hypertensive parents with a potential risk to develop high blood pressure.

Adolescent↗
PubMed1990

A new circulating hypertensive factor in the plasma of essential hypertensive subjects.

The pressor responses to dialyzed plasma extracts from normotensive (n = 15) and essential hypertensive (n = 14) human subjects were evaluated in anesthetized Sprague-Dawley rats. Hypertensive but not normotensive plasma raised mean arterial pressure (23.6 +/- 3.6 versus -0.5 +/- 2.5 mmHg, P less than 0.0001), and this effect was correlated significantly with its ability to stimulate 45Ca uptake in rat tail artery vascular smooth muscle (r = 0.883, P less than 0.002). These data suggest a humoral contribution to the pathophysiology of essential hypertension in at least some individuals. The time-course and molecular weight distribution of the dialyzed plasma suggest that this effect is not due to known vasopressor substances, but to a factor we tentatively term plasma hypertensive factor.

Animals↗
PubMed2004

The renin angiotensin system in childhood hypertension: selective increase of angiotensin-(1-7) in essential hypertension.

OBJECTIVE: We examined the activity of the renin-angiotensin system (RAS) in normotensive and hypertensive children. STUDY DESIGN: Hypertensive patients (12 with renovascular hypertension and 15 with essential hypertension) and 32 normotensive subjects were evaluated at a Pediatric Nephrology Center. Blood samples for plasma renin activity (PRA) and angiotensin peptides measurements were obtained once from normotensive subjects and before and after treatment from hypertensive patients. Plasma samples were extracted using Bond-Elut cartridges (Analytichem International, Harbor City, Calif), and peptide concentrations were determined by radioimmunoassay (RIA). RESULTS: PRA, Angiotensin I (Ang I), Angiotensin II (Ang II), and Angiotensin-(1-7) [Ang-(1-7)] levels were significantly higher in renovascular hypertensive patients than in normotensive children (3.3 +/- 1.2 vs 0.40 +/- 0.22 ng Ang I/mL/hour, 81.4 +/- 24.8 vs 26.4 +/- 13.4 pg/mL, 59.3 +/- 17.0 vs 21.4 +/- 8.7 pg/mL, 41.0 +/- 10.5 vs 16.2 +/- 7.9 pg/mL, respectively). The surgical treatment normalized blood pressure, PRA, and angiotensins levels. In contrast with renovascular disease, only Ang-(1-7) levels were significantly increased in essential hypertensive patients compared with normotensive (78.8 +/- 22.8 vs 16.2 +/- 7.9 pg/mL). Treatment with calcium channel blockers did not alter the RAS measurements. CONCLUSION: Our data show different RAS profiles in childhood hypertension and suggest a blood pressure-independent change of Ang-(1-7) in essential hypertension.

Adolescent↗
PubMed1997

Elevated albumin excretion in nonmodulating essential hypertensive patients.

Nonmodulating (NM) essential hypertensives are characterized by abnormal renal and aldosterone responses to angiotensin II. Recently, hyperinsulinemia, hypercholesterolemia, and an increased prevalence of family history of hypertension and myocardial infarction have been shown in NM hypertensives. Since an elevated urinary albumin excretion (UAE) has been indicated as a negative prognostic marker for cardiovascular diseases in essential hypertensives, we evaluated UAE in 50 male patients with mild to moderate essential hypertension (mean age 46.3 +/- 4.4 years), characterized as low renin (LR) (n = 14), modulating (M) (n = 20), and NM patients (n = 16) according to their renin profile and ability to modulate the aldosterone response to a graded infusion of angiotensin II. A group of 14 healthy male subjects (mean age 43.3 +/- 3.9 years) served as control. Resulting data showed that NM had significantly higher UAE (30.7 +/- 10.7 microg/min) than controls (11.9 +/- 2.7 microg/min, p < 0.0001), LR (22.1 +/- 8.4 microg/min, p < 0.05), and M patients (19.7 +/- 6.6 microg/min, p = 0.0001) when all fed a 200-mmol NaCl/day diet. On the contrary, differences in UAE disappeared when all subjects were on a low sodium regimen (10 mmol NaCl/day). Compared to LR and M patients, the NM ones also manifested higher low-density lipoprotein cholesterol levels (p < 0.05). Furthermore, these latter and UAE were positively correlated in NM patients (r = 0.579, p < 0.05) but not in the other subgroups. In conclusion, the current study demonstrates elevated UAE in NM patients, suggesting the NM phenotype is combined to an increased cardiovascular risk.

Adult↗