Development of blood pressure in spontaneously hypertensive rats after withdrawal of long-term treatment related to vascular structure

Christensen, Kent Lodberg; Jespersen, Lennard Tang; Mulvany, Michael J.

doi:10.1097/00004872-198902000-00002

Cited by 161 publications

(81 citation statements)

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“…In this simple experiment, the arteriolar hypertrophy was found to be significantly reduced in the ARB-treated rats compared with the CCB-treated rats, despite similar reductions in blood pressure ( Figure 2). Similar results have been reported by other groups using ACE inhibitors in both animal models, 16,62 and humans. 63,64 We also examined renal arteriolar structure in rats treated with highdose 'pulse' ARB therapy, and found a remarkable reversal of the arteriolar hypertrophy found in SHR treated with ARB, whereas this effect was not seen with CCB ( Figure 3).…”

Section: Role Of Renal Microvascular Protection In the Prevention Andsupporting

confidence: 91%

“…11,12 Studies from the group of Berecek suggested that these results could result from a decrease in AVP levels. 13,14 Similar studies have been performed by other laboratories using both ACE inhibitors, 15,16 and angiotensin receptor blockers (ARBs). 17,18 In our initial studies, we found that treatment of stroke-prone SHR with an ACE inhibitor from age 3-10 weeks resulted in a sustained suppression of blood pressure, whereas such an effect was not found with the vasodilator hydralazine.…”

Section: Animal Models Of Hypertension Preventionmentioning

confidence: 67%

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Prevention and regression of hypertension: role of renal microvascular protection

et al. 2009

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Hypertension is a disease which affects over 26.4% of the world adult population, therefore novel approaches to the prevention and treatment of this disease need to be examined. Previous studies from our and other laboratories have shown that treatment of spontaneously hypertensive rats (SHR) and Dahl salt-sensitive rats with a renin-angiotensin system (RAS) inhibitor during the 'critical period' in hypertension development results in prevention of the later development of hypertension. In humans, Julius et al. reported similar findings in the landmark TROPHY study. Recently, we reported that 'pulse' treatment of SHR with highdose angiotensin receptor blocker (ARB) is effective in causing sustained reduction of already established hypertension, even when the treatment was started after the 'critical period'. These results suggest the possibility that 'regression' of established hypertension may become feasible, and we have started a prospective, multicenter clinical study (STAR CAST study) to examine this possibility. In our animal studies, we found that treatment of rats during the 'critical period' with an ARB inhibits the development of renal arteriolar hypertrophy. Moreover, a high-dose angiotensin blocker caused a remarkable reversal of renal arteriolar hypertrophy in SHR, which was associated with changes in microvascular MMP expression. These results suggest that changes in the renal microvasculature may have an important role in the mechanisms of hypertension prevention and regression by ARB.

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Section: Role Of Renal Microvascular Protection In the Prevention Andsupporting

confidence: 91%

Section: Animal Models Of Hypertension Preventionmentioning

confidence: 67%

Prevention and regression of hypertension: role of renal microvascular protection

et al. 2009

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“…- 15 In the other two groups of treated SHR, the rise in blood pressure was to about 50% of the normal strain difference, which was similar to the earlier findings.…”

supporting

confidence: 90%

Enalapril can prevent vascular amplifier development in spontaneously hypertensive rats.

1990

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Three groups of spontaneously hypertensive rats (SHR) were given enalapril (25 mg/kg/day) from 4 to 9 weeks, 4 to 14 weeks, and 14 to 20 weeks of age. The drug was stopped and observations continued for another 16-21 weeks. At selected times, we measured blood pressure, in vitro hindquarter vascular resistance properties, left ventricular weight/body weight ratio, and skeletal muscle vessel norepinephrine kinetics in treated and untreated SHR and in Wistar-Kyoto (WKY) rats. At the end of each treatment period, all cardiovascular variables were close to values of WKY rats and well below those of untreated SHR, and the norepinephrine or fractional rate constant was about 25% below those levels. After enalapril was stopped, blood pressure and left ventricular weight/body weight ratio increased in parallel to levels ranging from 30% to 50% of the normal difference between untreated SHR and WKY rats. However, in SHR treated from 4 to 9 weeks and from 4 to 14 weeks of age, hindquarter resistance properties remained close to WKY rat levels for the entire observation period of 16-21 weeks after treatment, suggesting suppression of the enhanced resistance responses of SHR (amplifier properties). In SHR treated from 14 to 20 weeks of age, suppression of amplifier properties was more transient, and they redeveloped partially 5-6 weeks after cessation of therapy. When enalapril was given up to 14 weeks of age, the long-term suppression of amplifier properties was probably mainly through prevention of smooth muscle hypertrophy in resistance vessels and possibly through other mechanisms (eg., "rarefaction"). After that age, its therapeutic action was similar to that of other antihypertenslve drugs where, after drug withdrawal, there is a slow pressure rise in parallel with redevelopment of vascular and cardiac hypertrophy. (Hypertension 1990;16:252-260)

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“…Because of the novelty of the procedure, the rats were not left overnight to recover but were at all times kept under close observation. Previous experience 10 with Brietal anesthesia and surgery has shown complete recovery of all blood pressure parameters 4 to 5 hours after completion of the surgery. After induction of a second anesthesia, rats were killed by excising the heart.…”

Section: Methods Animalsmentioning

confidence: 89%

Perindopril changes the mesenteric pressure profile of conscious hypertensive and normotensive rats.

Christensen

Mulvany

1994

Hypertension

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Information about how antihypertensive therapy affects the arterial blood pressure profile in conscious animals is at present not available. Here we report measurements of part of the pressure profile in conscious spontaneously hypertensive rats (SHR, n=7) and Wistar-Kyoto (WKY, n=7) rats before and after treatment with the angiotensin-converting enzyme inhibitor perindopril. The previously developed technique that we used, provided simultaneous measurements of the undisturbed arterial blood pressure at the base of mesenteric arcades ( P^ diameter, approximately 100 nm) and systemic mean blood pressure (MBP). The ratio P

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Development of blood pressure in spontaneously hypertensive rats after withdrawal of long-term treatment related to vascular structure

Cited by 161 publications

References 0 publications

Prevention and regression of hypertension: role of renal microvascular protection

Prevention and regression of hypertension: role of renal microvascular protection

Enalapril can prevent vascular amplifier development in spontaneously hypertensive rats.

Perindopril changes the mesenteric pressure profile of conscious hypertensive and normotensive rats.

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