摘要:

The purpose of this study was to examine effects of hypertension on mechanics of cerebral arterioles in nongenetic and genetic models of chronic hypertension. Pressure (servo null) and diameter were measured in pial arterioles of anesthetized renal hypertensive rats (one-kidney, one clip), uninephrectomized nonnotensive rats, spontaneously hypertensive rats, and nonnotensive Wistar-Kyoto rats. During maximal dilatation with EDTA, external diameter of pial arterioles at 70 mm Hg pial arteriolar pressure was not significantly different in renal hypertensive and nonnotensive rats (86±5 [mean±SEM] versus 84±4 μm) but was less in spontaneously hypertensive rats than in Wistar-Kyoto rats (81±3 versus 92± μm;p<;0.05). Cross-sectional area of the arteriolar wall (hlstological) was greater in renal hypertensive than in nonnotensive rats (1.360±131 versus 952±89 μm2;p<0.05) and in spontaneously hypertensive rats than in Wistar-Kyoto rats (1,294±97 versus 817±86μm2;p<0.05). The stress-strain relation obtained from pressure-diameter data during maximal dilatation with EDTA indicated that distensibility of pial arterioles, when fully relaxed, was greater in renal hypertensive and spontaneously hypertensive rats than in nonnotensive and Wistar-Kyoto rats. We used point-counting stereology to quantitate composition of pial arterioles in renal hypertensive rats. Cross-sectional area of smooth muscle and elastin was significantly greater in renal hypertensive than in nonnotensive rats (smooth muscle, 947±108 versus 620±62μm2; elastin, 101±11 versus 55±6 μm2;p<0.05), whereas cross-sectional area of collagen and basement membrane was not significantly different in the two groups (collagen, 6±1 versus 5±1 μm2; basement membrane, 120±12 versus 104±8 μm2). Thus, we conclude that 1) cerebral arterioles undergo hypertrophy in both renal hypertensive and spontaneously hypertensive rats; 2) cerebral arterioles in renal hypertensive rats do not undergo “remodeling” with a reduction in external diameter, whereas external diameter is smaller in spontaneously hypertensive than in Wistar-Kyoto rats; 3) distensibility of cerebral arterioles, when fully relaxed, is increased in renal hypertensive rats and is greater in spontaneously hypertensive than in Wistar-Kyoto rats; and 4) the distensible components of the arteriolar wall are increased disproportionately in cerebral arterioles of renal hypertensive rats, which may contribute to increases in arteriolar distensibility.

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Angiotensin converting enzyme exists in two different isoforms, somatic and germinal, whose respective distributions and intracellular localizations have not been precisely determined. The differing biochemical and molecular characteristics of the two isozymes allowed the preparation of antibodies specific for each of the two angiotensin converting enzyme isoforms and of two nucleic acid probes, one of which was specific for the germinal isoform. Immunohistochemistry and in situ hybridization were used to determine the cell distribution of, respectively, the two isoforms and their corresponding messenger RNAs in the classically studied tissues of male adult humans and marmosets. Results provided by the two different methods were always concordant and were identical in the two species. The somatic angiotensin converting enzyme form was expressed uniquely in somatic tissues (vascular endothelial cells and at the brush border of renal proximal convoluted tubule, jejunal villus, and epididymal duct epithelia), and the germinal form was expressed uniquely in germinal cells with a precise stage-specific pattern, starting in round spermatids and finishing in spermatozoa. In situ hybridization documented the presence of somatic angiotensin converting enzyme messenger RNA in renal tubule epithelium, jejunal enterocytes, and epididymal epithelium and demonstrated that there was no direct correlation between the levels of angiotensin converting enzyme messenger RNA and the enzyme it encodes for, i.e., angiotensin converting enzyme, in a given epithelium. The significance of the ultraselective expression of germinal angiotensin converting enzyme and of its specific messenger RNA at a very precise stage of spennatogenesis remains uncertain.

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

This study aimed 1) to assess whether patients with an exaggerated blood pressure response to the doctor's presence (“white coat” effect) also display a pattern of enhanced blood pressure reactivity to mental stress and physical exercise and 2) to determine the presence of left ventricular structural and filling abnormalities in patients with white coat hypertension. We studied 56 (40 men) consecutive patients (mean [SD] age, 46.4 [9.1] years) whose clinic blood pressure was repeatedly high. Patients were classified as having white coat hypertension (n=20) if both their mean daytime (from 7 AM to 11 PM) ambulatory systolic and diastolic blood pressures were less than 134 and 90 mm Hg, respectively. Patients were considered to have persistent hypertension (n=36) if daytime systolic blood pressure was 134 mm Hg or more or diastolic blood pressure was 90 mm Hg or more. Eighteen subjects with clinic blood pressure lower than 140/90 mm Hg served as a normotensive control group. Blood pressure reactivity from baseline to mental arithmetic, isometric handgrip, and cycle ergometry did not display any difference among the three groups. The white coat hypertensive group had left ventricular mass index lower than the persistent hypertensive group but higher than the normotensive group. Doppler indexes of left ventricular diastolic filling displayed similar abnormalities in the white coat and persistent hypertensive groups compared with the normotensive group. We conclude that 1) we cannot distinguish white coat hypertensive patients by a pattern of blood pressure hyperreactivity to mental and physical laboratory tasks, and 2) white coat hypertension is characterized by mild cardiac enlargement and shares with persistent hypertension similar abnormalities in left ventricular filling. These latter findings suggest that white coat hypertension may not be considered an entirely innocuous clinical condition.

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

The present study was designed to analyze quantitatively the effects of a wide range of endothelin-1 levels on renal hemodynamlcs and renin release in the canine nonftltering kidney, including their effects on glomerular hydraulic pressure. Intrarenal infusion of endothelin-1 produced dose-dependent reductions in renal blood flow, but it did not affect glomerular hydraulic pressure until the infused dose reached high rates. At the rate of 1.0 ng/kg per minute, endothelin-1 reduced renal blood flow by 23% (p<0.01), whereas glomerular hydraulic pressure was not significantly changed from 68.1±1.3 to 67.4±1.2 mm Hg. However, with a higher rate of endothelin-1 infusion (5.0 and 10.0 ng/kg per minute), glomerular hydraulic pressure fell to 59.5±1.3 and 51.5±1.8 mm Hg (p<0.01), whereas renal blood flow was reduced from 154.5±15 to 83.0±9.5 and 53.5±9.9 mL/min, respectively. Endothelin-1 infusion also produced an inhibitory effect on renin release. With infusion at 1.0 ng/kg per minute, renin release fell from the control level of 47.9±5.6 to 26.6±4.9 units/min per gram kidney weight (p<0.01), and it fell further to 16.1±4.3 units/min per gram kidney weight with infusion at 10.0 ng/kg per minute. In summary, endothelin-1 infusion did not affect glomerular hydraulic pressure despite a fall in renal blood flow at low doses, but at high doses it reduced both, suggesting that endothelin-1 exerts separate, dose-dependent effects on preglomerular and postglomerular resistances. In addition, the present study demonstrated that endothelin-1 infusion has an ability to inhibit renin release in vivo when the macula densa-medlated pathway is eliminated.

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

To evaluate whether, in the forearm of hypertensive patients with different circulating renin profiles, local β-adrenergic receptor-induced production of active renin, plasma renin activity, angiotensin I (Ang I), and angiotensin II (Ang II) was or was not related to the renin profile, we studied four groups of patients: 1) hypertensive patients with primary aldosteronism and suppressed circulating plasma renin activity values (0.15±0.1 ng Ang I/mL per hour,n=7), 2) essential hypertensive patients with low (0.47±0.1 ng Ang I/mL per hour,n=8) circulating plasma renin activity values, 3) essential hypertensive patients with normal (2.48±0.52 ng Ang I/mL per hour;n=8) circulating plasma renin activity values, and 4) renovascular hypertensive patients with high circulating plasma renin activity values (4.16±2.1 ng Ang I/mL per hour;n=10). Isoproterenol was infused into the brachial artery, and active renin, plasma renin activity, and Ang I and Ang II forearm balance (venous-arterial differences corrected for forearm blood flow by strain-gauge plethysmography) were measured. Despite a comparable vasodilation, β-adrenergic stimulation failed to release active renin, plasma renin activity, and Ang I and Ang II in primary aldosteronism. It slightly increased them (except for Ang I) in low renin patients but determined a local production in normal renin and renovascular hypertensive patients. The individual increments in plasma renin activity and Ang II release induced by isoproterenol showed a correlation with the renin profile. In another group of essential hypertensive patients (n=6), isoproterenol was infused for 60 minutes, and we observed that despite a stable forearm vasodilation, both plasma renin activity and Ang II reached maximum values between 5 and 10 minutes; after that, they immediately started to decline and returned to basal levels. These data suggest the possibility that in hypertensive patients, vascular tissue renin originates from plasma uptake.

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Previously, we have reported two major αarradrenergic receptor transcripts in rat brain of 3.8 and 3.0 kb and the cloning and characterization of the rat brain complementary DNA (cDNA) (RBα2c) specific for the 3.0-kb messenger RNA. In this report, we used rat brain cDNAs specific for the 3.0 and 3.8 kb transcripts, which encode the α2cand α2a-adrenergic receptors, respectively, and the RNGα2cDNA, which encodes for the nonglycosytated α2b-adrenergic receptor in rat, to study tissue-specific expression of the three α2-adrenergic receptor genes in rat To eliminate cross-hybridization of probes with transcripts from other α2genes, we subcloned fragments that encode for the highly divergent third cytoplasmic loop of each rat α2-adrenergic receptor cDNA and used RNase protection analysis to detect specific transcripts. We show that the three rat α2-adrenergic receptor genes have diverse patterns of tissue expression, and although transcripts specific for each α2-adrenergic receptor gene are found in brain and kidney, the levels of expression of each subtype differ in these tissues. We speculate on the significance of tissue-specific expression of the α2-adrenergic receptor genes.

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

A validation study of the continuous noninvasive tonometric blood pressure monitor called JENTOW was performed in 20 normotensive subjects and 10 hypertensive patients. Tonometric and intra-arterial blood pressures were simultaneously recorded at supine rest and during a Valsalva maneuver and tilting test The results of the strict evaluation of the instrument's capacity for reproducing intra-arterial blood pressure were as follows: 1) The overall frequency response of the transcutaneous blood pressuremonitoring system based on arterial tonometry was flat, with negligible delay to intra-arterial blood pressure in the range of 0-5 Hz. 2) The largest discrepancy between intra-arterial and tonometric pressure waveforms was found at the early systolic phase; except for this phase, the tonometric waveform was almost equal to the intra-arterial waveform. 3) The beat-to-beat variability of tonometric pressure corresponded to that of intra-arterial pressure almost perfectly in the physiologically significant frequency range of 0–0.5 Hz. 4) During resting conditions, the averages of the systolic and diastolic values measured tonometrically corresponded well to those measured intra-arterially. 5) The changes in the betweenmethod discrepancy of blood pressure values during the Valsalva maneuver were statistically significant but small (<5 mm Hg). 6) No significant effect of postural tilting was found on the between-method discrepancy. We conclude that this method is clinically acceptable and reliable except for its limited capacity for recording the higher frequency intra-arterial waveform and for responding to the relatively rapid and large transient changes in blood pressure.

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

To evaluate the influence of salt sensitivity on the blood pressure response to oral indomethacin treatment, we studied 35 hospitalized essential hypertensive patients (24 men and 11 women, aged from 40 to 55 years). During a normal NaCl intake (120 mmol Na+per day), patients were assigned to receive in a randomized double-blind fashion either 200 mg indomethacin (25 patients) or placebo (10 patients) for 5 days. Two weeks after the interruption of indomethacin treatment, during which the normal NaCl intake was continued, salt sensitivity was assessed by giving each patient a high (220 mmol Na+per day for 10 days) and then a low (20 mmol Na+per day for 10 days) NaCl diet Blood pressure changes were evaluated, and the measurement taken at the end of the 2 weeks under normal sodium intake was considered baseline blood pressure. Patients were classified as salt sensitive when a diastolic blood pressure change of 10 mm Hg or more occurred after both low and high periods of sodium intake. In salt-resistant patients treated with indomethacin (n=12, nine men and three women, mean age 50.5±3.7 years), neither blood pressure (systolic blood pressure from 150.8±11.2 to 154.6±9.3 mm Hg, NS; diastolic blood pressure from 99.3±2.1 to 101.1±4.4 mm Hg, NS) nor the urinary Na+excretion (from 108.1±20.9 to 97.9±9.1 mmol/24 hr, NS) was significantly affected by the drug. On the contrary, when compared with patients receiving placebo (five men and five women, mean age 44.4±4.1 years), salt-sensitive hypertensive patients (n=13, 10 men and three women, mean age 47.9±6.5 years) showed significantly higher levels (p<0.004) of diastolic blood pressure after indomethacin therapy. According to these data, compared with pretreatment values blood pressure significantly increased in salt-sensitive patients after indomethacin treatment (systolic blood pressure from 156.9±9.7 to 163.5±10.8 mm Hg,p<0.001; diastolic blood pressure from 98.5±2.1 to 105.7±5.7 mm Hg,p<0.006) despite a marked plasma renin activity (from 0.18±0.14 to 0.10±0.09 ng/L per second,p<0.02) and aldosterone (from 390.5±154.9 to 299.3±169.5 pmol/L,p<0.002) decrease. Salt-sensitive patients also showed a significant indomethacin- related decrease of urinary Na+excretion (from 108.1±11.6 to 90.9±10.1 mmol/24 hr,p<0.04). Our results indicate that the blood pressure response to indomethacin depends on salt sensitivity in human essential hypertensive patients. The increase of blood pressure, observed in salt-sensitive hypertensive patients, is followed by a significant reduction in urinary Na+excretion. This finding suggests that the indomethacin-induced decrease in Na+excretion is responsible for the blood pressure increase showed by salt-sensitive patients after oral indomethacin treatment.

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1993

数据来源: OVID