摘要:

We evaluated the mechanical properties of the carotid artery in anesthetized Dahl rats with or without long-term treatment with the diuretic compound indapamide. The mechanical properties of the carotid artery were evaluated by establishing pressure-volume curves in situ in vivo before and after total relaxation of arterial smooth muscle by potassium cyanide. Dahl salt-sensitive and salt-resistant rats were fed either a low (0.4%) or high (7%) NaCl diet for 5 weeks. In each group, half the rats received for the same period of time oral treatment with indapamide (3 mg/kg per day). Blood pressure, heart rate, and pressure-volume curves were studied at the end of the 5-week period. In untreated Dahl salt-sensitive rats, the pressure-volume curve of the carotid artery was shifted to the right compared with that in untreated Dahl salt-resistant rats. The finding was observed even after potassium cyanide and regardless of the NaCl diet (P < .01 between Dahl salt-sensitive and -resistant rats). Indapamide was able to prevent the development of hypertension in Dahl salt-sensitive rats receiving a high NaCl diet (185 plus/minus 7 versus 146 plus/minus 8 mm Hg in untreated and treated Dahl salt-sensitive rats with a high NaCl diet, P < .0005). In the other groups, indapamide had no effect on blood pressure. Indapamide treatment increased carotid arterial static compliance in Dahl salt-sensitive rats with a high or low NaCl diet and to a lesser extent in Dahl salt-resistant rats. The increase was observed even after total relaxation of carotid arterial smooth muscle by potassium cyanide. These results suggest that (1) the mechanical properties of the carotid arteries were altered in Dahl salt-sensitive rats independently of NaCl diet and transmural pressure changes, and (2) the diuretic compound indapamide prevented the disturbed mechanical properties of the carotid artery in Dahl salt-sensitive rats with a high or low NaCl diet, acting on both arterial structure and function. Sodium sensitivity (and not sodium intake) influences the changes in the carotid artery mechanical properties of Dahl rats. (Hypertension. 1995;25:272-277.)

ISSN:0194-911X    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

We previously reported that adenosine has significant depressor effects in the nucleus tractus solitarii and area postrema of the rat. The purpose of this study was to determine whether the spontaneously hypertensive rat (SHR) has abnormalities in medullary sensitivity to adenosine. Male SHR and Wistar-Kyoto (WKY) rats (aged 12 to 15 weeks) were anesthetized with urethane, and blood pressure was monitored intraarterially. Stereotaxic microinjection (60 nL) of adenosine was made into the nucleus tractus solitarii and the area postrema and was confirmed histologically. Dose-related decreases in mean blood pressure and heart rate occurred in both strains tested, and this effect was completely abolished by 1,3-dipropyl-8-p-sulfophenylxanthine (0.92 nmol), a potent adenosine receptor antagonist. However, there were significant differences between SHR and WKY rats in the magnitude of blood pressure and heart rate depression. A similar pattern of response was found in the area postrema. Thus, adenosine is a potent depressor agent in the nucleus tractus solitarii and area postrema of rats, and adenosine has significantly fewer depressor effects in SHR. These data suggest that alterations in purinergic mechanisms of central cardiovascular control exist in the SHR model. (Hypertension. 1995;25:278-282.)

ISSN:0194-911X    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

This study examined the effect on mean blood pressure of a new orally active nonpeptide angiotensin II (Ang II) receptor antagonist, EXP 3174, in doses that completely block exogenous Ang II action. Anesthetized and conscious two-kidney, two clip chronic renovascular hypertensive rats and sham-operated animals were used. In anesthetized hypertensive rats, intracerebroventricular administration of the inhibitor had no effect on blood pressure, whereas blood pressure was normalized by intravenous injection of the antagonist (163 plus/minus 12 to 110 plus/minus 9 mm Hg, P < .05). In sham anesthetized rats, intravenous injection of EXP 3174 also lowered blood pressure (112 plus/minus 6 to 96 plus/minus 6 mm Hg, P < .05). In conscious rats, intravenous EXP 3174 induced a fall in pressure that was larger in hypertensive (156 plus/minus 9 to 132 plus/minus 5 mm Hg, P < .05) than in sham (104 plus/minus 3 to 94 plus/minus 4 mm Hg, P < .05) rats. Plasma renin activity was very high in anesthetized animals (hypertensive versus sham, 87.8 plus/minus 8.3 versus 95.7 plus/minus 10.2 ng Ang I/mL per hour); differences were not significant either between anesthetized hypertensive and sham or in conscious animals (hypertensive versus sham, 9.42 plus/minus 1.58 versus 6.74 plus/minus 2.32 ng Ang I/mL per hour). Angiotensinogen concentration was higher in cerebrospinal fluid in anesthetized hypertensive rats (36.4 plus/minus 3.0 versus 26.0 plus/minus 2.4 ng Ang I/mL, P < .05) and in the artery wall of hypertensive conscious rats (103.1 plus/minus 10.3 versus 75.2 plus/minus 7.8 ng Ang I/g, P < .05). In summary, the central renin-angiotensin system does not seem to participate in the maintenance of high blood pressure in hypertensive animals. The enzymatic system present in the vascular wall appears to be activated in hypertensive rats. The hypotensive effect of EXP 3174 suggests that Ang II could be one of the factors involved in the maintenance of two-kidney, two clip hypertension. (Hypertension. 1995;25:283-287.)

ISSN:0194-911X    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Phase II of two-kidney, one clip (2K1C) Goldblatt hypertension in the rat is characterized by elevated blood pressure and near-normal plasma concentrations of angiotensin II (Ang II) but is reversed by inhibition of the renin-angiotensin system. We hypothesized that this angiotensin dependence is due to enhanced responsiveness to the slow pressor effect of Ang II caused by renal artery stenosis. To test this idea, we submitted rats to either renal artery clipping or sham operation. These groups were immediately subdivided; some animals received enalapril in their drinking water (508 micro mol/L), and the rest drank distilled water only. After 10 to 14 days, catheters were inserted into the aorta and vena cava, and the rats were housed in metabolism cages. After 3 control days of measurement of mean arterial pressure and other variables, the enalapril-treated groups received an intravenous infusion of Ang II at a dose of 3.8 pmol/min (4 ng/min) for 14 days. Rats not drinking enalapril received only saline vehicle (2 mmol Na+per day). After 3 days of Ang II infusion, the enalapril-treated 2K1C rats had attained a significantly higher level of mean arterial pressure than the enalapril-treated sham rats. At the end of the Ang II infusion, mean arterial pressure in enalapril-treated 2K1C rats was 151 plus/minus 6 mm Hg versus 107 plus/minus 7 mm Hg in enalapril-treated sham rats. Mean arterial pressure in the enalapril-treated sham rats after Ang II infusion was not significantly different from that of untreated sham rats (109 plus/minus 2 mm Hg). No significant differences in urinary sodium excretion or water balance were noted between the 2K1C and sham rats. These results support the hypothesis that 2K1C rats exhibit enhanced responsiveness to the slow pressor effect of Ang II. (Hypertension. 1995;25:288-293.)

ISSN:0194-911X    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The objective of this study was to assess individual responses to antihypertensive treatment by N-of-1 trials using blood pressure self-monitoring in 79 patients of both sexes referred to a hypertension clinic. Thirty-five patients who remained untreated (study 1) and 44 N-of-1 trial participants (study 2) were consecutively selected if their clinic blood pressure was between 160/95 and 220/115 mm Hg and there were no hypertensive complications. Blood pressure was measured daily at home for 21 days (three consecutive measures, morning and evening). Each N-of-1 trial was a single-blind treatment consisting of two successive 10-day treatment pairs, each pair comprising 5 days of placebo followed by 5 days of 20 mg enalapril once daily in the morning. Study 1 showed no significant blood pressure regression toward the mean over 20 days and justified the choice of 5-day treatment periods in study 2. In study 2, blood pressure fell significantly 12 hours after the first administration of enalapril and rose within 24 hours of the end of the 5-day active treatment period. Using evening blood pressure values (12 hours after enalapril intake) from the first treatment pair, 33 patients were classified as responders (diastolic blood pressure fall greater or equal to 6 mm Hg). In 16 of these 33 patients, the fall in blood pressure above 6 mm Hg was not maintained in the morning, 24 hours after drug intake. Response reproducibility was tested by comparison with the second treatment pair: the observed agreement was only 0.71 (chance-corrected agreement: 0.34) when defined according to both evening and morning values. N-of-1 trial methodology can be useful for decision making in the care of individual patients. It can be based on the use of home blood pressure determinations, provided that there are at least 30 readings in each 5-day trial period. The individual agreement between the antihypertensive responses to two successive enalapril treatment periods is only moderate and is not sufficient to justify using this design for performing in individual patients randomized comparison of an angiotensin-converting enzyme inhibitor and another antihypertensive drug. (Hypertension. 1995;25:294-301.)

ISSN:0194-911X    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1995

数据来源: OVID