Tissue Converting Enzyme Activity Is Low in the Kidney of Spontaneously Hypertensive Rats

Welsch, C; Em, Giesen-Crouse; Schmidt, Mary J.; Jl, Imbs

doi:10.1097/00005344-198706107-00027

Cited by 5 publications

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“…It is of interest to note that the kidney ACE activity in the hypertensive animals was lower than that seen in kidneys of the normotensive WKY rats. This has been reported previously [38,39]. The most dramatic effect of chronic Fig.…”

Section: Discussionsupporting

confidence: 78%

The Effect of Captopril Treatment and Its Withdrawal on the Gene Expression of the Renin-Angiotensin System

1994

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The mRNA expression of renin, angiotensinogen and angiotensin converting enzyme (ACE) was determined in the kidneys and livers from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) during chronic treatment with captopril and following its withdrawal. Chronic captopril treatment was associated with a dramatic rise in renin mRNA in the kidney and an elevation in mRNA for ACE in the liver. The release from captopril treatment was associated with a reversal of the increase in kidney renin mRNA but no reversal of the sustained elevation of ACE mRNA in the liver. In situ hybridisation revealed a localisation of renin to the area of the juxtaglomerular apparatus in the kidneys from untreated animals, but recruitment of vascular sites of renin expression in kidneys from captopril-treated animals. In kidneys from released animals, renin mRNA expression was once again confined to the juxtaglomerular apparatus. ACE mRNA was expressed in hepatocytes throughout the livers from animals in all treatment groups. The results highlight a differential effect of captopril withdrawal upon the gene expression of the components of the renin-angiotensin system in kidney and liver.

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Section: Discussionsupporting

confidence: 78%

The Effect of Captopril Treatment and Its Withdrawal on the Gene Expression of the Renin-Angiotensin System

1994

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“…[13][14][15] For example, previous studies have also shown that the expression and activity of ACE are reduced in the developing SHR kidney. 11 In addition, renal renin activity and renal Ang I and Ang II concentrations are elevated before the onset of hypertension in the SHR kidney. 13,14 The expression of the angiotensin receptor is also increased 15 from as early as 4 weeks of age, associated with increased responsiveness to Ang II.…”

Section: Discussionmentioning

confidence: 99%

“…Renal ACE activity was reduced at PN-1 in SHRs compared to WKY rats, as previously described in this model. 11…”

Section: Expression Of Ace2 and Ace At Pn-1mentioning

confidence: 99%

Developmental expression of ACE2 in the SHR kidney: A role in hypertension?

Tikellis

Cooper

Bialkowski

et al. 2006

Kidney International

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The abnormal development of the intrarenal renin-angiotensin system (RAS) is thought contribute to adult-onset hypertension in the spontaneously hypertensive rat (SHR). Angiotensin-converting enzyme 2 (ACE2) is a novel enzyme with complementary actions to that of ACE. Recent studies have shown that ACE2 expression is reduced in the adult SHR. However, its regulation in pre-hypertensive animals is unknown. In this study, we examine the developmental expression of ACE2 in the rodent kidney and its temporal expression, as it relates to the development of hypertension in the SHR model. Kidneys from SHR and normotensive Wistar Kyoto (WKY) rats (n=8-12/group) at birth, 6 weeks of age, and adulthood (80 days) were examined. Gene expression and activity of ACE2 were determined by real-time reverse transcription-polymerase chain reaction and quenched fluorescence assays, respectively. Renal expression was localized by in situ hybridization and immunohistochemistry. The expression and ACE2 activity are significantly increased in the SHR kidney at birth. With the onset of hypertension, the tubular expression of ACE2 falls in SHR compared to WKY and remains reduced in the adult SHR kidney. Glomerular expression is paradoxically increased in the SHR glomerulus. The overall developmental pattern of ACE2 expression in the SHR kidney is also modified, with declining expression over the course of renal development. The developmental pattern of ACE2 expression in the SHR kidney is altered before the onset of hypertension, consistent with the key role of the RAS in the pathogenesis of adult-onset hypertension. Further research is required to distinguish the contribution of these changes to the development and progression of hypertension in this model.

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“…Because, in this animal model which has been used as an appropriate experimental model for the human essential hypertension, the renin-angiotensin system is normal or even suppressed both in plasma (Koletsky et al 1970;Freeman et al 1975;Shiono & Sokabe 1976) and tissues (PolskyCynkin et al 1980;Welsch et al 1987) except that vascular renin is reportedly elevated (Antonaccio et al 1981). Cohen and Kurz (1982) have proposed that vascular tissue is a potential target site for the antihypertensive action of ACE inhibitors, based on their finding that an ACE inhibitor exerted a prolonged suppression of ACE activity in aorta of SHR while the enzyme activity in plasma was rapidly restored.…”

Section: Introductionmentioning

confidence: 99%

“…Similarly, it is also controversial as to how inhibitors of renin (Miyazaki et al 1976) and of ACE (Unger et al 1990) lower BP in spontaneously hypertensive rats Correspondence: Hideki Okunishi, MD, Department of Pharmacology, Osaka Medical College, 2-7 Daigakumachi,Takatsuki,569,Japan. (SHR) developed by Okamoto and his group (Oka-mot0 & Aoki 1963). Because, in this animal model which has been used as an appropriate experimental model for the human essential hypertension, the renin-angiotensin system is normal or even suppressed both in plasma (Koletsky et al 1970;Freeman et al 1975;Shiono & Sokabe 1976) and tissues (Polsky-Cynkin et al 1980;Welsch et al 1987) except that vascular renin is reportedly elevated (Antonaccio et al 1981). Cohen and Kurz (1982) have proposed that vascular tissue is a potential target site for the antihypertensive action of ACE inhibitors, based on their finding that an ACE inhibitor exerted a prolonged suppression of ACE activity in aorta of SHR while the enzyme activity in plasma was rapidly restored.…”

Section: Introductionmentioning

confidence: 99%

Pathogenetic Role of Vascular Angiotensin‐converting Enzyme in the Spontaneously Hypertensive Rat

Okunishi

Kawamoto

Kurobe

et al. 1991

Clin Exp Pharma Physio

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1. This study was undertaken to examine the possibility that the level of angiotensin-converting enzyme (ACE) increases in vascular tissue, and that this may participate in the pathogenesis of hypertension in spontaneously hypertensive rat (SHR). 2. In SHR, at the established hypertensive stage, the prolonged antihypertensive effect induced by a single oral dose of spirapril was closely correlated to the long-lasting inhibition of ACE in aortae and mesenteric arteries. In contrast, ACE in plasma, lung, heart and kidney recovered from inhibition faster than in vessels. 3. Prolonged daily oral treatment of SHR with spirapril, initiated at the age of 8 weeks and continued for 8 weeks, prevented the development of hypertension with concomitant decrease in aortic ACE activity. Blood pressure continued to be suppressed after the drug was withdrawn, as did the aortic ACE activity. 4. Spontaneously hypertensive rats developed hypertension with age as well as with the increase in aortic ACE activity which became higher with age than that of Wistar-Kyoto (WKY) normotensive control rats. On the contrary, ACE activity in plasma and lung of SHR was substantially lower than that of WKY at any age from 4 to 20 weeks old. Brain ACE activity of SHR did not differ from that of WKY at any age. Aged SHR showed the lower enzyme activity in the kidney compared with that of age-matched WKY. 5. Our results support the hypothesis that increased vascular ACE may play an essential role in the development and maintenance of hypertension in SHR.

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Tissue Converting Enzyme Activity Is Low in the Kidney of Spontaneously Hypertensive Rats

Cited by 5 publications

References 0 publications

The Effect of Captopril Treatment and Its Withdrawal on the Gene Expression of the Renin-Angiotensin System

The Effect of Captopril Treatment and Its Withdrawal on the Gene Expression of the Renin-Angiotensin System

Developmental expression of ACE2 in the SHR kidney: A role in hypertension?

Pathogenetic Role of Vascular Angiotensin‐converting Enzyme in the Spontaneously Hypertensive Rat

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