Plasma renin activity and changes in tissue angiotensin converting enzyme

Michel, Bruno; Grima, Michèle; Stephan, Dominique; Coquard, Catherine; Welsch, C; Barthelmebs, Mariette; Imbs, Jean-Louis

doi:10.1097/00004872-199405000-00011

Cited by 27 publications

(21 citation statements)

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“…In summary, taken together the most significant changes observed in the present work and previous information [17,20,21], it could be hypothesized that in the renal cortex there is an increased formation of Ang II, a reduction in its metabolism and an increased formation of Ang IV in the non-clipped kidney of G2K1C animals. On the other hand, valsartan treatment suggests an increased formation of Ang II together with a decreased metabolism of Ang III in the renal cortex of normal rats and in the clipped kidney of G2K1C animals (Fig.…”

Section: Discussionsupporting

confidence: 74%

“…SOL AspAP activity was also reduced in the clipped, but not in the non-clipped kidney of G2K1C rats. The non-clipped kidney did not show variation in ACE activity, whereas the clipped kidney exhibited increased ACE activity compared with Sham-operated rats [17]. Taken together, these results suggest an inhibition of the metabolism of Ang I through the Ang 2-10 pathway favoring Ang II production following treatment with valsartan and the kidney stenosis.…”

Section: Discussionmentioning

confidence: 68%

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Angiotensinase activities in the kidney of renovascular hypertensive rats

et al. 2003

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In spite of the well-known contribution of angiotensin II (Ang II) in the pathogenesis of Goldblatt two-kidney one clip (G2K1C) hypertension, the importance of other Ang peptides, such as Ang III, Ang IV or Ang 2-10, is scarcely understood. The functional status of these peptides depends on the action of several aminopeptidases called angiotensinases. The metabolism of Ang III to Ang IV by aminopeptidase M (AlaAP) and of Ang I to Ang 2-10 by aspartyl aminopeptidase (AspAP) was evaluated in the renal cortex and medulla of normotensive (Sham-operated) and hypertensive (G2K1C) rats, treated or not with the AT 1 receptor antagonist valsartan. The results demonstrated a highly significant increase of membrane-bound (MEMB) AlaAP in the cortex of the non-ischemic kidney of G2K1C rats compared with the kidney of normal rats and with the clipped kidney of G2K1C rats. This suggests an increased formation of Ang IV in the non-clipped kidney of G2R1C rats. Valsartan reduced MEMB AlaAP and AspAP activities in the renal cortex of normotensive and in the clipped kidney of hypertensive rats. The reduced metabolism of Ang III may prolong its half-life in valsartan-treated animals. These results suggest a role for AlaAP in renovascular hypertension. In addition, the higher AspAP activity of the renal cortex compared to medulla reflects its relative functional difference between both locations.

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 68%

Angiotensinase activities in the kidney of renovascular hypertensive rats

et al. 2003

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“…For example, some studies in normotensive mice (Tamura et al, 1998), Wistar-Kyoto rats (Kreutz et al, 1995), and rodent models of hypertension (Michel et al, 1994;Zhao et al, 2000) have indicated that tissue ACE expression is increased with high salt intake. In contrast, other studies in rats (Fox et al, 1992;Michel et al, 1994) indicate that tissue ACE expression is unchanged or decreased during high salt intake. The mechanism through which salt intake modulated serum ACE activity in the present study is not known, but it could involve effects of sodium on tissue ACE expression, cleavage and secretion of ACE, or ACE enzyme activity.…”

mentioning

confidence: 99%

Loss of Sodium Modulation of Plasma Kinins in Human Hypertension

Murphey

Eccles²,

Williams³

et al. 2004

J Pharmacol Exp Ther

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We studied the effect of salt intake and hypertension on the systemic kallikrein-kinin system (KKS), as measured by bradykinin (BK) 1-5, a stable circulating bradykinin metabolite, and the tissue KKS, as measured by urinary kallikrein excretion. Venous BK 1-5, urinary kallikrein, and components of the reninangiotensin-aldosterone system were measured in 35 normotensive and 19 hypertensive subjects who were maintained on a high (200 mmol/day) or low (10 mmol/day) salt diet. Salt restriction decreased mean arterial pressure (MAP) (P Ͻ 0.001 overall) and the plasma angiotensin-converting enzyme (P ϭ 0.017) and increased plasma renin activity (P Ͻ 0.001) and serum aldosterone (P Ͻ 0.001). There was an interactive effect of salt intake and hypertension on plasma BK 1-5 (P ϭ 0.043), with BK 1-5 significantly lower during low compared with high salt intake in normotensive (24.7 Ϯ 2.6 versus 34.9 Ϯ 5.6 fmol/ml, P ϭ 0.002) but not hypertensive subjects (30.6 Ϯ 4.6 versus 27.5 Ϯ 2.8 fmol/ml, P ϭ 0.335). In normotensives, the change in plasma BK 1-5 from high to low salt intake correlated with the change in MAP (r ϭ 0.533, P ϭ 0.004). Urinary kallikrein was higher during low compared with high salt intake (P Ͻ 0.001) in both groups. There was no effect of salt intake on urinary BK 1-5. In summary, the systemic and renal KKSs act in tandem to modulate the response to salt intake. The systemic system is activated during high salt intake and counterbalances increased vascular response to pressors. With sodium restriction, the renal system is activated and counterbalances the increased sodium-retaining state induced by activation of the renin-angiotensin-aldosterone system. With hypertension, these modulating effects are diminished or lost, supporting a role for both systems in the development/maintenance of hypertension.

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“…PRA and AGT were measured exactly as described previously (37). Briefly, PRA was determined by the ability of circulating renin to generate Ang I from circulating AGT, during a 30-min incubation of plasma at 37°C.…”

Section: Measurement Of Pra and Plasma Agtmentioning

confidence: 99%

“…In both cases, the conversion of Ang I into Ang II was inhibited by the addition of a cocktail of peptidase inhibitors. Ang I thus generated was then measured by RIA using rabbit anti-Ang I. Antibodies to Ang I were raised in rabbits that were immunized against the peptide coupled to BSA by carbodiimide condensation (37). PRA and AGT concentrations are expressed as nanograms of Ang I generated per milliliter of plasma and per hour of incubation.…”

Section: Measurement Of Pra and Plasma Agtmentioning

confidence: 99%

Intravenous Delivery of PTH/PTHrP Type 1 Receptor cDNA to Rats Decreases Heart Rate, Blood Pressure, Renal Tone, Renin Angiotensin System, and Stress-Induced Cardiovascular Responses

Fritsch

Lindner²,

Welsch³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. While parathyroid hormone type 1 receptor (PTH1R)-mediated vasodilatory, cardiac stimulatory, and renin-activating effects of exogenous PTH/PTH-related protein (PTHrP) are acknowledged, interactions of endogenous PTHrP with these systems remain unclear, mainly because the unavailability of viable PTHrP/PTH1R knockout mice. Transgenic mice overexpressing PTH1R in smooth muscle strongly have supported the PTHrP/PTH1R system as a cardiovascular system (CVS) regulator, but the consequences on renovascular (RVS) and renin-angiotensin systems (RAS) have not been explored in these studies. The aim was to develop a model in which one could study the consequences on CVS, RVS, and RAS of generalized PTH1R overexpression. Systemic PTH1R cDNA plasmid delivery was used in adult rats, a system that is amenable to studies in isolated perfused kidneys and that minimizes development-induced compensatory mechanisms. Intravenous administration of hPTH1R or green fluorescence protein-tagged hPTH1R in pcDNA3 resulted 3 wk later, in generalized expression of hPTH1R (mRNA and protein), especially in vessels, liver, heart, kidney, and central nervous system, where it is expressed physiologically. As expected, PTH1R overexpression decreased BP and renal tone. Unexpected, however, PTH1R overexpression decreased heart rate. These studies also revealed that endogenous PTHrP actually inhibits renin release and that hPTH1R overexpression tends to increase that effect. Striking, liver production and circulatory level of angiotensinogen and hence plasma renin activity were markedly reduced. Thus, abrupt PTH1R overexpression in adult rats profoundly alters the CVS, RVS, and RAS, strongly supporting the PTH/PTHrP/PTH1R system as crucial for heart and vascular tone regulation. In addition, these results revealed that PTH1R-mediated mechanisms might have protective effects against cardiovascular stress-induced responses, including stimulations in heart rate and RAS.

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Plasma renin activity and changes in tissue angiotensin converting enzyme

Cited by 27 publications

References 0 publications

Angiotensinase activities in the kidney of renovascular hypertensive rats

Angiotensinase activities in the kidney of renovascular hypertensive rats

Loss of Sodium Modulation of Plasma Kinins in Human Hypertension

Intravenous Delivery of PTH/PTHrP Type 1 Receptor cDNA to Rats Decreases Heart Rate, Blood Pressure, Renal Tone, Renin Angiotensin System, and Stress-Induced Cardiovascular Responses

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