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J Ménard

Publications and source records attributed to J Ménard.

At least 37 records · Page 2Linked to original sources
PubMed1999

The international database of self-recorded blood pressures in normotensive and untreated hypertensive subjects.

OBJECTIVES: To pool data from individual subjects in an attempt to determine an operational threshold for making clinical decisions based on the self-recorded blood pressure (SRBP) and to examine how many hypertensive subjects, diagnosed by conventional blood pressure (CBP) measurement, would have a self-recorded blood pressure within the normotensive range if the proposed thresholds were applied. DATA SOURCES: Thirteen research groups studied 4668 untreated subjects. RESULTS: In total 2401 subjects were normotensive, 494 were borderline hypertensive and 1773 were definitely hypertensive. Hypertension had been diagnosed from the mean of 1-6 (median 3) CBP measurements obtained during 1-3 (median 1) visits. The reference values for SRBP measurements determined from the 95th percentiles of the distributions for normotensive subjects were 137 mmHg systolic and 85 mmHg diastolic. Of the subjects with systolic hypertension, 16% had systolic SRBP </= 137 mmHg. Similarly, 25% of those with diastolic hypertension had diastolic SRBP </= 85 mmHg. The probability that hypertensive subjects had SRBP below these thresholds was 34% (diastolic) to 62% (systolic) greater for women than it was for men, was 2-3 times greater if fewer than three CBP measurements had been averaged for establishing the diagnosis of hypertension, and increased by 50% (diastolic) to 126% (systolic) when SRBP had been measured on more than 3 days. In contrast, for each 10 mmHg increment in systolic CBP, this probability decreased by 35% for systolic SRBP and by 11% for diastolic SRBP; for each 5 mmHg increment in diastolic CBP it decreased by 36% for diastolic SRBP. In addition, for systolic blood pressure, the probability decreased by 31% for each 10-year increment in age. CONCLUSIONS: Until the relationship between SRBP and the incidence of cardiovascular morbidity and mortality has been clarified further by prospective studies, a mean self-recorded blood pressure above 137 mmHg systolic or 85 mmHg diastolic may be considered hypertensive. Among the hypertensive patients 16-31% had SRBP below these thresholds, but this proportion decreased if the hypertensive subjects had higher CBP.

Adolescent↗
PubMed1999

[Audit of the treatment of arterial hypertension in specialized consultation].

The objective of the study was to estimate the control of elevated blood pressure (BP) among patients regularly followed-up and to analyse physicians attitudes in patients having uncontrolled BP. Two hundred and fifty-eight consecutive patients (mean age 56 years, 58% of males) with essential hypertension attending the outpatient department of a specialised hypertension clinic, having at least a 6-month follow-up at the clinic and at least 3 prior visits, were included in the study. Twelve different physicians were in charge of these patients. Data were collected [1] from the structured computerised record called ARTEMIS and [2] from a structured questionnaire filled up by the physician after each visit, where he/she explained the reasons for his/her decisions. BP was measured by a nurse using an automatic device (oscillometric method) and then by a physician using a mercury sphygmomanometer. During follow-up, mean physician's BP fell from 179/107 to 148/91 mmHg and mean nurse BP fell from 164/96 to 143/83 mmHg. Percentages of patients having a controlled hypertension (BP < 140/90 mmHg) were 27% (physician's BP) and 45% (nurse BP). Physicians did not modify treatment in 59% of patients among whom they measured a BP > or = 140/90 mmHg. The 3 main reasons given by physicians for not modifying treatment were: BP controlled when using other BP measurement methods (nurse, home or ambulatory BP), 44%; BP control considered as satisfactory, 29%; systolic hypertension in the elderly, 8%. The person (physician or nurse) who measures BP and the measurement method have dramatic consequences on BP control level. Reasons for not modifying treatment in uncontrolled patients (physician's BP > or = 140/90 mmHg) were based on opinions rather than evidence, for example when isolated systolic hypertension in the elderly is concerned.

Adult↗
PubMed1998

Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. HOT Study Group.

BACKGROUND: Despite treatment, there is often a higher incidence of cardiovascular complications in patients with hypertension than in normotensive individuals. Inadequate reduction of their blood pressure is a likely cause, but the optimum target blood pressure is not known. The impact of acetylsalicylic acid (aspirin) has never been investigated in patients with hypertension. We aimed to assess the optimum target diastolic blood pressure and the potential benefit of a low dose of acetylsalicylic acid in the treatment of hypertension. METHODS: 18790 patients, from 26 countries, aged 50-80 years (mean 61.5 years) with hypertension and diastolic blood pressure between 100 mm Hg and 115 mm Hg (mean 105 mm Hg) were randomly assigned a target diastolic blood pressure. 6264 patients were allocated to the target pressure < or =90 mm Hg, 6264 to < or =85 mm Hg, and 6262 to < or =80 mm Hg. Felodipine was given as baseline therapy with the addition of other agents, according to a five-step regimen. In addition, 9399 patients were randomly assigned 75 mg/day acetylsalicylic acid (Bamycor, Astra) and 9391 patients were assigned placebo. FINDINGS: Diastolic blood pressure was reduced by 20.3 mm Hg, 22.3 mm Hg, and 24.3 mm Hg, in the < or =90 mm Hg, < or =85 mm Hg, and < or =80 mm Hg target groups, respectively. The lowest incidence of major cardiovascular events occurred at a mean achieved diastolic blood pressure of 82.6 mm Hg; the lowest risk of cardiovascular mortality occurred at 86.5 mm Hg. Further reduction below these blood pressures was safe. In patients with diabetes mellitus there was a 51% reduction in major cardiovascular events in target group < or =80 mm Hg compared with target group < or =90 mm Hg (p for trend=0.005). Acetylsalicylic acid reduced major cardiovascular events by 15% (p=0.03) and all myocardial infarction by 36% (p=0.002), with no effect on stroke. There were seven fatal bleeds in the acetylsalicylic acid group and eight in the placebo group, and 129 versus 70 non-fatal major bleeds in the two groups, respectively (p<0.001). INTERPRETATION: Intensive lowering of blood pressure in patients with hypertension was associated with a low rate of cardiovascular events. The HOT Study shows the benefits of lowering the diastolic blood pressure down to 82.6 mm Hg. Acetylsalicylic acid significantly reduced major cardiovascular events with the greatest benefit seen in all myocardial infarction. There was no effect on the incidence of stroke or fatal bleeds, but non-fatal major bleeds were twice as common.

Aged↗
PubMed1998

[Home blood pressure monitoring].

Home blood pressure measurement is a simple, precise and highly reproducible method. Its application is possible in a large majority of patients. The method is valid if performed with devices validated according to international criteria and if an appropriate methodology is applied. It is advantegeously used for diagnostic of high blood pressure, particularly white coat hypertension. It allows for an exact appreciation of treatment efficacy and a long term follow-up of blood pressure control. In a majority of patients it improves their compliance to drug treatment. Its precision allows to decrease the number of patients needed in clinical trials. The main obstacle of larger use of home blood pressure monitoring is the need to give a detailed instructions to patients and generally a laborious evaluation of results. The latter could be simplified by using devices transferring measured results directly to physician's computer. However the cost of such instruments remains high. Finally the lack of financial reimbursement of physicians using home blood pressure measurement limits further its larger use.

Blood Pressure Monitors↗
PubMed1998

Prevalence, treatment, and control of hypertension in the French population: data from a survey on high blood pressure in general practice, 1994.

A survey was conducted in a cohort of 235 general practitioners (GP) selected by Sofres Medical who were representative of the French medical population, to measure the percentage of patients with hypertension, treated hypertensives and patients with controlled hypertension. Data were collected over 1 week of office consultation. Practitioners were initially instructed to use the same type of mercury sphygmomanometer, equipped with pneumatic cuffs of different sizes. Three consecutive blood pressure (BP) measurements were made and the last two were recorded. Practitioners had to carry out their own survey over a period of 1 week on all patients > 18 years of age who visited their offices. Patients were considered as hypertensive (HP) if the mean of the two recorded BP measurements was > or = 140/90 mm Hg or if they were taking antihypertensive drug treatment. Three cutoff points were used to define controlled hypertension: < 140/90 mm Hg (overall population of HP), < 160/95 mm Hg (HP < 65 years of age), and < 160/90 mm Hg (HP > or = 65 years of age). Among 12,351 patients (mean age, 48.6 years; women, 58%), 5020 were HP, (41%) of whom 2035 were without treatment (41%) and 2985 were receiving antihypertensive drug treatment (59%). Two hundred-thirty patients (4.6%) remained at high risk with moderate or severe hypertension (BP > or = 180 [systolic] or 105 [diastolic] mm Hg), ie, 1 patient/week/GP. The study confirms the high prevalence of hypertension in general practice and shows that 7 of 10 patients have an acceptable control of their BP (< 160/95 or < 160/90 mm Hg according to age) but only 24% of treated HP achieved the target of a BP level < 140/90 mm Hg, representing 28% of the 18 to 64 year old group and 21% of the elderly group. French GP did not choose an optimal control, and the medical community is waiting for answers to crucial questions, ie, does optimal BP control significantly improve the absolute cardiovascular risk? How far should blood pressure be lowered?

Antihypertensive Agents↗
PubMed1998

An attempt to improve blood pressure control in the French population: information and outcome awareness at the general practitioner level.

To improve blood pressure (BP) control in general practice, 3122 general practitioners agreed to participate in a result awareness program. A survey carried out 6 months after participating physicians had been informed of the outcome of treatments they had given showed that blood pressure control (cut-off point: BP < 140/90 mm Hg) had not improved. However, using less stringent criteria, a slight improvement in blood pressure control could be observed. Although this improvement was marginal, results are sufficiently encouraging to warrant another study after a new awareness campaign among the medical population.

Adult↗
PubMed1998

Mouse and rat plasma renin concentration and gene expression in (mRen2)27 transgenic rats.

The (mRen2)27 transgenic rat [TGR(mRen2)27] is said to have low plasma levels of active renin. We used a direct radioimmunoassay (RIA) for mouse submaxillary renin, as well as an indirect enzyme-kinetic assay based on the generation of angiotensin I with modification of the pH optimum, to measure rat and mouse plasma renin activity (PRA), plasma renin concentration (PRC), and plasma prorenin in TGR before and after lisinopril. The relationship between rat PRC and % rat kidney extract was steepest at pH 6.0 and flat at pH 8.5, whereas the relationship between mouse PRC and purified mouse renin was steepest at pH 8.5 and flat at pH 6.0. Mouse PRC was highly correlated with direct RIA measurements (r = 0.93). PRA before lisinopril was little influenced by pH, whereas the increase with lisinopril was greatest at pH 6.5. PRC before lisinopril was fourfold higher at pH 8.5 compared with that at pH 6.0. Lisinopril increased both PRC values but reversed the pH dependency. Prorenin was fourfold higher at pH 8.5 compared with that at pH 6.0 and decreased slightly with lisinopril. Renal renin concentration was higher at pH 6.0 than at pH 8.5. With lisinopril, renal renin concentration increased at both pH values. Mouse PRC was not changed by lisinopril. Ribonuclease protection assay showed both rat and mouse renin gene expression in the kidney, which increased with lisinopril. Thus TGR have circulating active rat and mouse renin and prorenin. The notion that TGR are a "low renin" model should be revised.

Angiotensinogen↗
PubMed1998

Additive effects of enalapril and losartan in (mREN-2)27 transgenic rats.

Blockade of angiotensin II AT1 receptors combined with angiotensin I-converting enzyme inhibition might amplify the potency of the renin-angiotensin system blockade. We studied whether chronic and simultaneous administration of enalapril and losartan would result in additive or synergistic effects in the (mREN-2)27 transgenic rat (TGR), the investigated targets being blood pressure, cardiac hypertrophy, renin-angiotensin system blockade achieved, and plasma active renin concentration. In addition, the origin (renal or extrarenal, rat or mouse) of the induced renin release was determined. Adult TGRs were treated orally and daily for 5 to 7 weeks with 1 mg/kg (E1) or 3 mg/kg (E3) enalapril or 1 mg/kg (L1) or 3 mg/kg (L3) losartan, or their combinations (E1L1 and E3L3). At the end of the treatment period, enalapril and losartan exerted dose-dependent and, when combined, additive effects in terms of blood pressure fall and cardiac hypertrophy limitation, and synergistic effects in terms of plasma active renin stimulation and blockade of exogenous angiotensin I pressor effects, with E3L3>E3>L3, E1L1>E1> or =L1, and E1L1=E3>L3). This indicates that in the TGR, (1) the greater the renin-angiotensin system blockade achieved, the greater are the reduction in blood pressure, the limitation of cardiac hypertrophy, and the reactive rise in plasma renin concentration elicited, and (2) the enalapril-losartan combinations are more potent at achieving these goals than any of their constituents individually. In contrast, there was no interaction between the two drugs regarding aldosteronuria reduction. Measurement of plasma renin concentration and renal renin at pH 6.5 and 8.5, ie, the optimal pH values for rat and mouse renin activities, respectively, indicates that in TGRs the counterregulatory process for renin release elicited by enalapril, losartan, or their combination involves primarily rat renin of renal origin, a finding supported further by the observed increase in the rat renal renin hybridization index.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Superiority of home blood pressure measurements over office measurements for testing antihypertensive drugs.

OBJECTIVE: To compare the effects on office blood pressure and home blood pressure of placebo and active drug administration. DESIGN: After a 2-week wash-out period, patients with mild-to-moderate hypertension entered a 2-week single-blind placebo period and then a 4-week double-blind period. Patients were randomly assigned to be administered either 2 mg trandolapril once daily or its placebo in a 2:1 proportion. Office blood pressure was measured by a physician at the end of each period, using a mercury sphygmomanometer (mean of three consecutive measurements). Home blood pressure was measured during the last week of each period according to standard procedure carefully taught to each patient by the physician. Compliance was checked by using electronic pill boxes. RESULTS: Data for 34 of the 44 patients who entered the study were eligible for analysis. Baseline systolic blood pressure/diastolic blood pressure were significantly (P = 0.0001/P = 0.0001) higher for office blood pressure (161/101 mmHg) than they were for home blood pressure (145/93 mmHg). There was no statistically significant difference between the placebo and active-treatment groups at baseline. During the single-blind period, blood pressures measured at the office and at home did not change significantly. Office blood pressure decreased by 2.7 +/- 10 mmHg for systolic blood pressure and by 0.5 +/- 4 mmHg for diastolic blood pressure whereas home blood pressure increased by 0.8 +/- 6 mmHg for systolic blood pressure and by 0.7 +/- 4 mmHg for diastolic blood pressure. During the double-blind period, office blood pressure fell significantly with trandolapril treatment (systolic by 10.2 +/- 12 mmHg, diastolic by 8.3 +/- 6 mmHg; P = 0.0005/0.0001, versus single-blind placebo period) but this decrease was not significantly different (P = 0.45/0.92) from the fall in members of the placebo group (systolic by 6.9 +/- 9 mmHg, diastolic by 8.0 +/-6 mmHg; P = 0.04/0.002, versus single-blind placebo period). Thus, no antihypertensive effect of trandolapril was demonstrated. The fall lin home blood pressure with trandolapril treatment was significant (systolic by 10.7 +/- 8 mmHg, diastolic by 5.8 +/- 5 mmHg; both P = 0.0001, versus single-blind placebo period) and was significantly greater (P = 0.0004/0.004) than the minimal change observed with placebo (systolic fell by 0.2 +/- 5mmHg, diastolic fell by 0.6 +/- 4 mmHg; P = 0.90/0.62, respectively, versus single-blind placebo period). The evening decrease in home blood pressure was similar to the morning decrease in home blood pressure in members of the trandolapril-treated group. The resulting morning:evening decrease in blood pressure ratio was 0.83 for diastolic blood pressure and 0.95 for systolic blood pressure. For the subgroup of responders, mean of individual ratios was 0.77 +/- 0.43 for diastolic blood pressure and 0.70 +/- 0.39 for systolic blood pressure. CONCLUSION: The placebo effect observed with office blood pressure measurements does not occur with home blood pressure measurements. Expected treatment effect can alter a physician's blood pressure readings. The precision of measurements is greater with home blood pressure (there is a lower SD). Use of home blood pressure measurements increases the power of comparative trials, allowing one either to study fewer subjects or to detect a smaller difference in blood pressure.

Journal Article↗
PubMed1998

Angiotensin I-converting enzyme inhibition but not angiotensin II suppression alters angiotensin I-converting enzyme gene expression in vessels and epithelia.

The concentration of angiotensin-converting enzyme (ACE) increases during chronic treatment with ACE inhibitors for unknown reasons. We investigated whether alterations in ACE mRNA and ACE concentration occur in the different tissues during ACE inhibition and the role of angiotensins in these regulations by comparing ACE inhibitors with other blockers of the renin-angiotensin system. Enalapril, an ACE inhibitor, in the range of 0.3 to 10 mg/kg/day in rats induced dose- and time-dependant increases in plasma ACE up to two to three times control values. There were significant increases in the steady state ACE mRNA in the lung (32%), duodenum (64%) and aorta (324%) and 40% to 140% increases in membrane-bound enzyme concentration in these tissues and in the heart and kidney. The ACE content of purified duodenal brush border was increased by 80%, but the enzyme and its mRNA in the testis were not altered. The angiotensin II receptor antagonist losartan at several regimens of up to 30 mg/kg twice a day for 14 days produced no change in plasma ACE level or lung ACE mRNA. The human renin inhibitor ciprokiren was tested in guinea pigs, a species sensitive to this compound. Both enalapril and cilazapril induced 2-fold increases in plasma ACE, but ciprokiren (24 mg/kg/day for 12 days) had no effect. Enalapril treatment of BN/Kat rats (lacking circulating kininogens) caused a similar increase in ACE as in other rats. This study documents a general increase in ACE gene expression and enzyme concentration in tissues during ACE inhibition, with the exception of the testis, most probably reflecting an activation of the 5', so-called somatic promoter of the ACE gene. Angiotensins are not involved in this regulation and do not seem to control ACE gene expression in normal rodents.

Angiotensin Receptor Antagonists↗
PubMed1998

[Can echocardiography identify mildly hypertensive patients at high risk, left untreated, based on current guidelines?].

OBJECTIVE: To determine if the decision to treat uncomplicated mild hypertension with drugs, in accordance with the WHO/ISH guidelines based on a series of blood pressure (BP) measurements over six months, resulted in the treatment of patients at high risk, on the basis of echocardiography. BACKGROUND: The value of echocardiography in mild hypertension management remains is unclear. METHODS: One hundred and eighteen patients with mild hypertension (90 to 105 mmHg diastolic BP and/or 140 to 180 mmHg systolic BP) were examined by echocardiography at inclusion and followed up for 6 months by a single physician unaware of the echographic results. RESULTS: Drug treatment was given to 48 patients, and 70 remained untreated. Treated patients had higher echographic indices than untreated patients (all p < 0.05): LV mass/body surface area (82.8 +/- 15.9 vs 74.7 +/- 15.0 g/m2), interventricular septal thickness (9.7 +/- 1.7 vs 8.5 +/- 1.3 mm). LV posterior wall thickness (8.4 +/- 1.1 vs 7.8 +/- 1.1 mm), relative wall thickness (0.37 +/- 0.06 vs 0.34 +/- 0.06). Left ventricular (LV) geometry was normal in 98 patients, and 20 had LV concentric remodeling. The 10-year coronary disease risk (Framingham equation) was higher in treated patients than in untreated patients (10.0% vs 6.3%; p < 0.002), and in the 20 patients with concentric remodeling than in those with normal LV geometry (10.4%) vs 4.2%; p < 0.005). Nine of these 20 patients were still untreated at the end of the six-month follow-up period. CONCLUSION: Rigorous application of the WHO-ISH clinical guidelines in a group of mild hypertensive patients, led to the treatment of patients with slightly higher LV mass and more concentric LV geometry than were found in those not treated. However, a high-risk subgroup, with concentric remodeling, was not identified and left untreated.

Adult↗
PubMed1998

[Do WHO-ISH guidelines identify high risk mild hypertensive patients?].

OBJECTIVE: To assess the ability of 1993 WHO-ISH recommendations to identify patients who need drug treatment. METHODS: 268 hypertensive patients with suspected mild hypertension were preselected for this study at their first visit at the referral center. 123 were included after a short in-hospital work-up when they fulfilled the 1993 WHO-ISH criteria for mild hypertension (90-105 mmHg diastolic BP and/or 140-180 mmHg systolic BP). Echocardiography was performed in all patients by the same investigator according to ASE convention. The combined 10-year risk of stroke and coronary heart disease was calculated with the Framingham equation. Patients were then followed up for six months by the same physician blinded to echographic results and risk calculations and applying the WHO-ISH guidelines (monthly BP measurement and subjective assessment of risk). Five patients were excluded, for reasons unrelated to the protocol. RESULTS: The decision of drug treatment was taken at the 1st, 2nd, 3rd, 4th, 5th, 6th monthly visit after work-up in 2, 6, 25, 7, 2 and 6 patients, respectively. Among these 118 patients, 48 patients (29 male, 19 female) were eventually treated and 70 (49 male, 30 female) remained untreated. BP s at preselection and on a day of work-up were similar in both groups. Patients in whom drug treatment was prescribed were older and had higher lef ventricular mass (LVM) than untreated patients, but only 2 of them (all in the treated group) had LVM values above usual thresholds (LVM > 125 g/m2, in men and women). Stroke and coronary risks were both higher in treated than in untreated patients (p < 0.05). The physician using the guidelines decided to treat only 19 of the 38 patients with a 10-year risk < 10% (true positive), whereas she decided to treat with drugs 12 patients among the 44 with a 10-year risk < 5%. CONCLUSION: The difference in LVM between untreated and treated patients support the validity of the WHO-ISH guidelines, but the measurement of LVM did not bring much information for managing the individual patient. Application of these guidelines did not satisfactorily identify high risk patients and could lead to over-treatment of low risk patients.

Aged↗
PubMed1997

Synergistic effects of ACE inhibition and Ang II antagonism on blood pressure, cardiac weight, and renin in spontaneously hypertensive rats.

BACKGROUND: Blockade of type 1 angiotensin (Ang) II receptors combined with ACE inhibition may amplify the efficacy of the renin-angiotensin system blockade because ACE inhibitors do not completely and permanently suppress Ang II production. METHODS AND RESULTS: Enalapril or losartan (1, 3, 10, and 30 mg/kg) or their combination was administered for 2 to 4 weeks to spontaneously hypertensive rats. The combination of low doses of each agent induced greater reductions in blood pressure (BP) and left ventricular weight/body weight (LVW/ BW) ratio than monotherapy with the same or higher doses. When approximately equipotent regimens of enalapril, losartan, and their combination, as judged by BP fall, were compared, there were similar increases in plasma and renal renin and in plasma Ang-(1-7) and Ang I and similar reductions in plasma angiotensinogen. Enalapril alone reduced plasma Ang II levels, and losartan alone increased Ang II levels. The combination of enalapril with losartan prevented or reduced the increase in Ang II levels observed with losartan alone. CONCLUSIONS: These findings show that the synergistic interaction between the effects of low doses of enalapril and losartan on BP and LVW/BW ratio is due to more effective inhibition of the renin-angiotensin system by their combination than by either agent alone. When both drugs are given together, the ACE inhibitor-induced fall in plasma Ang II results in modulation of the Ang II antagonist-induced reactive rise in Ang II, thereby lowering the plasma Ang II concentration, which competes with the antagonist for the Ang II receptors.

Angiotensin Receptor Antagonists↗
PubMed1997

High human renin hypertension in transgenic rats.

We developed a model of spontaneously high human renin hypertension in the rat by producing two transgenic strains, one for human angiotensinogen with the endogenous promoter and one for human renin with the endogenous promoter. Neither transgenic strain was hypertensive. These strains were then crossed, producing a double transgenic strain. The double transgenic rats, both males and females, developed severe hypertension (mean systolic pressure, 200 mm Hg) and died after a mean of 55 days if untreated. The rats had a human plasma renin concentration of 269 +/- 381 (+/-SD) ng angiotensin I (Ang I)/mL per hour, plasma renin activity of 177 +/- 176 ng Ang I/mL per hour, rat angiotensinogen concentration of 1.49 +/- 1 microgram Ang I/mL, and human angiotensinogen concentration of 78 +/- 39 micrograms Ang I/mL (n = 49). Control rats had plasma renin activity of 3.7 +/- 3.9 ng Ang I/mL per hour and rat angiotensinogen of 1.32 +/- 0.16 micrograms Ang I/mL. Angiotensinogen transgene expression by RNase protection assay was ubiquitously present but most prominent in liver. Renin transgene expression was high in kidney but absent in liver. The rats featured severe cardiac hypertrophy, with increased cross section of cardiomyocytes but little myocardial fibrosis. The kidneys showed atrophic tubules, thickened vessel walls, and increased interstitium. Both the angiotensin-converting enzyme inhibitor lisinopril and the specific human renin inhibitor remikiren lowered blood pressure to normal values. Double transgenic mice have been developed that exhibit features quite similar to those described here; their gene expressions are similar. The specificity of rodent and human renin is similarly documented. Although many elegant physiological studies can now be done in mice, rats nevertheless offer flexibility, particularly in terms of detailed cardiac and renal physiology and pharmacology. We conclude that this double transgenic strain will facilitate simultaneous investigation of genetic and pathophysiological aspects of renin-induced hypertension. The fact that human renin can be studied in the rat is a unique feature of this model.

Angiotensinogen↗