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Biomedical subjects

A Bobik

Publications and source records attributed to A Bobik.

At least 55 records · Page 3Linked to original sources
PubMed1995

Multiple types of ryanodine receptor/Ca2+ release channels are expressed in vascular smooth muscle.

Functional studies on vascular smooth muscle suggest the presence of ryanodine receptors (RyRs) with differing properties. In an attempt to understand such differences we investigated, using reverse transcription-polymerase chain reaction (RT-PCR), the possibility that smooth muscle cells express multiple types of RyRs. RNA was extracted from rat aorta, superior and small mesenteric arterial vessels, purified aortic smooth muscle media, or cultured aortic smooth muscle cells for cDNA synthesis. The cDNAs encoding RyR1, RyR2, and RyR3 were amplified using PCR primers based on sequences close to the 3' coding region of the RyR genes and PCR products verified by restriction endonuclease analysis. All three members of the RyR gene family were found to be present in vascular smooth muscle. This finding of multiple types of RyRs expressed in the same cell type indicates a complex mechanism of RyR Ca2+ channel regulation involving the formation of homo- and/or heterotetrameric complexes.

Animals↗
PubMed1995

Expression of growth factor receptors in arterial smooth muscle cells. Dependency on cell phenotype and serum factors.

The effects of modulation of rabbit aortic smooth muscle cells (SMCs) from the 'contractile' phenotype on surface membrane receptors binding epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) and platelet-derived growth factor-BB (PDGF-BB), as well as their responsiveness to these growth factors was investigated in cell culture. Cells predominantly of the 'contractile' phenotype expressed low numbers of high affinity EGF and bFGF receptors (EGFr: 1.09 +/- 0.18 fmol/10(6) cells; bFGFr: 0.32 +/- 0.07 fmol/10(6) cells). Upon modulation from the 'contractile' phenotype, the expression of these cell surface receptors increased greatly: 8- and 11-fold with respect to EGF and bFGF receptors. Cell surface receptors binding [125I]-PDGF-BB were largely unaltered. The elevated bFGF receptor number appeared dependent on SMC modulation from the 'contractile' phenotype and serum; the latter factor did not influence EGF receptor numbers. In both instances the increase in receptor numbers was independent of the proliferation status of the cells. Cells expressing high levels of the growth factor receptors also rapidly entered the cell cycle, proliferated, and exhibited growth factor-specific changes in shape in the presence of these growth factors. Because the effects on growth factor receptor numbers were observed in confluent cells, such alterations, are likely to play a significant role in vessel remodelling following balloon catheter angioplasty, in atherosclerotic vessels and the vascular hypertrophy associated with hypertension.

Animals↗
PubMed1995

Cardiovascular development after enalapril in spontaneously hypertensive and Wistar-Kyoto rats.

We studied the long-term effects after withdrawal of enalapril, an angiotensin-converting enzyme inhibitor, on tail systolic pressure and cardiovascular structural properties in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Observations in control rats were from 4 to 35 weeks of age, whereas treated rats received enalapril from 4 to 20 weeks and were studied for a further 15 weeks. We measured blood pressure and the ratio of left ventricle weight to body weight and derived methoxamine log dose-perfusion pressure curves in the isolated hindquarter bed. From the changes in resistance properties we also estimated the changes in structure using a model developed previously. During therapy, blood pressure was depressed to a common value in both strains. After drug withdrawal, by age 35 weeks, previously treated SHR developed only mild hypertension, whereas blood pressure of WKY had recovered to the corresponding control level. At 21 weeks, soon after enalapril was stopped, left ventricular development was depressed in both strains; the depression was slightly greater in SHR, but that of vascular resistance was proportionately similar in each strain. Late cardiovascular development between 21 and 35 weeks was attenuated in the previously treated groups. For the left ventricle, it was similar in each strain, but for the vasculature, late development was relatively smaller in SHR than WKY. In the former, the pattern of development between 21 and 35 weeks was the same as in untreated controls and appeared to be mediated in response to the rise in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Nongenomic effects of aldosterone on intracellular Ca2+ in vascular smooth muscle cells.

Genomic mechanisms of steroid action have been increasingly elucidated over the past four decades. In contrast, rapid steroid actions have been widely recognized only recently, and detailed analysis of the mechanisms involved are still lacking. The present article describes rapid effects of mineralocorticoid hormones on free intracellular calcium in vascular smooth muscle cells as determined by fura 2 spectrofluorometry in single cultured cells from rat aorta. These effects are almost immediate and reach a plateau after only 3 to 5 minutes and are characterized by high specificity for mineralocorticoids versus glucocorticoids. The potent mineralocorticoids aldosterone and fludrocortisone are agonists with estimated apparent EC50 values of approximately 0.1 to 0.5 nmol/L; deoxycorticosterone acetate is an agonist with an EC50 of approximately 5 nmol/L; and progesterone, cortisol, corticosterone, and estradiol have much lower potency (EC50 values of approximately 0.5 to 5 mumol/L). The effect of aldosterone is blocked by neomycin and short-term treatment with phorbol esters but augmented by staurosporine, indicating an involvement of phospholipase C and protein kinase C. The Ca2+ effect appears to involve the release of intracellular Ca2+, as shown by the inhibitory effect of thapsigargin; intriguingly, a relatively small maximum effect (approximately 40 nmol/L increase) is consistently seen. This mechanism operates at physiological subnanomolar aldosterone concentrations and appears to be a likely candidate for rapid fine tuning of cardiovascular responsivity. It may also contribute to known clinical features of mineralocorticoid action that are difficult to explain by the traditional genomic mechanism alone.

Aldosterone↗
PubMed1995

[Do glycoproteins IIb/IIIa participate in activation of human platelet s by low density lipoproteins?].

Low density lipoproteins (LDL) enhance the entry of Ca2+ and other bivalent cations via receptor-operated channels. The use of a synthetic peptide and antibodies blocking the glycoproteins IIb and IIIa interaction with ligands revealed that fibrinogen receptor antagonists prevent platelet aggregation without any effect on the ability of LDL to increase the cytoplasmic Ca2+ level. These data indicate that glycoproteins IIb-IIIa are not involved in the activation of the second messenger system by LDL but play a role in the proaggregant effect of LDL by providing cell-to-cell interactions.

Blood Platelets↗
PubMed1995

Transforming growth factor-beta 1 and the development of vascular hypertrophy in hypertension.

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional cytokine capable of regulating the growth and differentiation of many cell types, as well as regulating their environment in the blood vessel wall. Its production by endothelium and/or vascular smooth muscle is stimulated by biophysical forces, growth factors and also vasoconstrictors. In hypertension TGF-beta 1 gene transcription is most likely elevated by a combination of physical and chemical stimuli with the cytokine acting to increase the production of extracellular matrix proteins or to modulate smooth muscle cellular growth, producing hypertrophy, polyploidy or proliferation. With respect to the latter, TGF-beta 1 potentiates the proliferative effects of many receptor tyrosine kinase-activating growth factors in vascular smooth muscle from SHR, but inhibits such proliferation in WKY smooth muscle. It also differentially affects collagen production by the two cell types. It is suggested that the augmented proliferative response in renal hypertensive SHR, compared to renal hypertensive WKY, is the consequence of these differential effects of TGF-beta 1 on smooth muscle cell proliferation. TGF-beta 1 is also likely to be a significant contributor to the development of vascular hypertrophy in genetic hypertension.

Animals↗
PubMed1995

Intracellular pH in vascular smooth muscle: regulation by sodium-hydrogen exchange and multiple sodium dependent HCO3- mechanisms.

OBJECTIVES: The aim was to determine the mechanisms, particularly bicarbonate dependent mechanisms, of intracellular pH (pHi) recovery from various acidoses in vascular smooth muscle and to explore the ATP dependency of the respective mechanisms. METHODS: Experiments were conducted in rat aortic smooth muscle cells grown in primary culture and synchronised in a non-growing state by serum deprivation. pHi was measured in cells loaded with the pH sensitive fluorescent dye, 2',7'-bis-(2-carboxyethyl)-5-(and 6)-carboxyfluorescein (BCECF). Chloride efflux was studied by determination of the rate of efflux of 36Cl over 5 min. Cells were ATP depleted by substitution of glucose in the medium by 2-deoxyglucose. Acidoses were induced by CO2 influx and NH3 efflux techniques. RESULTS: In the absence of HCO3-, the 5-(N-ethyl-N-isopropyl) amiloride (EIPA) sensitive Na+/H+ exchange accounted for the recovery from intracellular acidosis. In the presence of HCO3- ions the response to respiratory acidosis (CO2 influx) was predominantly via activation of Na+/H+ exchange and an EIPA sensitive Na+ and HCO3- dependent mechanism. A 4-acetamido-4'-isothiocyanostilbene-2',2'-sulphonic acids (SITS) sensitive Na+ dependent Cl-/HCO3- mechanism which is also sensitive to EIPA makes a small contribution during severe intracellular acidosis. Under such conditions HCO3- dependent mechanisms contributed about 40% to the overall pHi regulating capacity of vascular smooth muscle cells. However, under conditions which deplete cellular ATP these pHi regulating mechanisms account for virtually all of theses cells' ability to regulate pHi. The inability of Na+/H+ exchange to participate in pHi recovery under these circumstances, reduces the ability of vascular smooth muscle cells to recover pHi by approximately 50-60%. Chloride efflux was approximately linear over 5 min and was increased by 36% in the presence of extracellular HCO3-. Efflux in the presence of HCO3- was inhibited similarly by both SITS and EIPA. CONCLUSIONS: At least three transporters contribute to recovery from acidosis in vascular smooth muscle: Na+/H+ exchange, an Na(+)-HCO3- cotransporter which is sensitive to EIPA, and an Na+ dependent HCO3-/Cl- exchange sensitive to both SITS and EIPA. The Na(+)-HCO3- cotransporter appears to be similar to that described in human vascular smooth muscle. When the Na+/H+ exchanger is attenuated by cellular ATP depletion, the alternative pathways, particularly the Na(+)-HCO3- cotransporter, ensure that substantial pHi regulatory capacity is maintained.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1995

Developmental regulation of transforming growth factor-beta 1 responses and vascular smooth muscle growth in spontaneously hypertensive rats.

OBJECTIVE: To investigate the developmental regulation of transforming growth factor-beta 1 (TGF-beta 1) action and the expression of TGF-beta receptors in vascular smooth muscle cells (VSMC) isolated from spontaneously hypertensive rats (SHR). DESIGN: TGF-beta 1 effects on proliferation and expression of TGF-beta receptor subtypes were compared in VSMC prepared from SHR, Wistar-Kyoto (WKY) and Sprague-Dawley rats of different ages. METHODS: TGF-beta 1 effects on platelet-derived growth factor-BB (PDGF-BB)-stimulated proliferation were examined in VSMC isolated from SHR, WKY and Sprague-Dawley rats aged 1, 4 and 12 weeks, and from renal hypertensive WKY rats. TGF-beta receptors on the surface of VSMC were identified by affinity labelling, followed by immunoprecipitation with TGF-beta receptor antibodies; complexes were then analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. RESULTS: TGF-beta 1 inhibited by 60-80% PDGF-BB-stimulated proliferation of VSMC from 1-week-old SHR. In 4-week-old SHR, VSMC were resistant to the antiproliferative action of TGF-beta 1, whereas the mitogenic activity of PDGF-BB was increased approximately 150% by TGF-beta 1 in VSMC from 12-week-old SHR. In contrast, TGF-beta 1 inhibited by 10-50% PDGF-BB-stimulated proliferation of VSMC from age-matched WKY and Sprague-Dawley rats. TGF-beta isoforms (TGF-beta 1, -beta 2, -beta 3) all elicited similar growth responses in VSMC from SHR and WKY rats of different ages. Hypertension per se did not alter TGF-beta 1 effects on proliferation, as TGF-beta 1 inhibited by 30-40% growth factor action on VSMC from control, uni-nephrectomized and one-kidney one-clip hypertensive WKY rats. The type I, II and III TGF-beta receptors were expressed on the surface of VSMC isolated from SHR of different ages. CONCLUSION: Alterations in TGF-beta 1 responses, which become evident in VSMC from 4-week-old SHR and are most prominent at 12 weeks, may be important in the development of vascular hypertrophy in this rat strain.

Aging↗
PubMed1994

Transforming growth factor-beta 1 regulates the expression of ryanodine-sensitive Ca2+ oscillations in cardiac myocytes.

Factors which regulate sarcoplasmic reticulum (SR) gene expression are largely unknown. We investigated whether Transforming Growth Factor-beta 1 (TGF-beta 1) plays a role in the maintenance of Ca2+ handling mechanisms in isolated neonatal rat cardiomyocytes. Myocytes cultured in the presence of serum were found to beat continuously and undergo spontaneous Ca2+ oscillations whereas in the absence of serum the cells lost the ability to undergo cyclical Ca2+ oscillations. The oscillations were restored when serum-free medium was supplemented with TGF-beta 1. Both caffeine-induced Ca2+ elevations and the inhibitory effect of ryanodine on spontaneous activity were also dependent on the continued presence of TGF-beta 1; in its absence these indices of SR function were severely compromised. TGF-beta 1 therefore appears to play a critical role in the maintenance of Ca2+ oscillations in the heart by regulating the expression of the ryanodine-sensitive Ca2+ release mechanism.

Animals↗
PubMed1994

Renin-angiotensin system in neonatal rats: induction of a renal abnormality in response to ACE inhibition or angiotensin II antagonism.

In experiments designed to analyze cardiovascular structure in response to antihypertensive therapy with an ACE inhibitor, we decided to start very early in life with the aim to prevent blood pressure increases and the development of vascular structural changes. In these treated groups of rats we unexpectedly observed that after they were weaned, their water consumption and urine volume, respectively, increased substantially. The present study was designed to determine if inhibition of the renin-angiotensin system produced similar effects in different strains of rats, and focused on characterizing the abnormal fluid balance occurring as a consequence to neonatal treatment with ACE inhibitors or angiotensin II blockers. Three-day-old Wistar Kyoto (WKY), Wistar (WR) and spontaneously hypertensive rats (SHR) were given either saline, enalapril, captopril, losartan and the AT2 blocker, PD123319, in the same amount of volume for 20 days. Treatment was stopped and rats were examined with regard to renal morphology at 4, 14 and 30 weeks of age. In addition, water consumption, urine volume, urine electrolytes and osmolality were analyzed at 14 weeks of age, that is, 10 weeks off treatment. Early treatment with the ACE inhibitors, enalapril and captopril, and the AT1 blocker, losartan, but not the AT2 blocker, PD 123319, in the SHR and in the normotensive strains WKY and WR produced persistent, irreversible histopathological renal abnormalities in adult life, long after the rats had been taken off treatment. These abnormalities consisted of mainly cortical tubulointerstitial inflammation, various degrees of papillary atrophy and pelvic dilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1994

Rat aortic smooth muscle cells expressing charybdotoxin-sensitive potassium channels exhibit enhanced proliferative responses.

1. The relationship between the expression of potassium (K+) channels and the growth properties of cultured vascular smooth muscle cells was examined. 2. Two groups of cells having different proliferative rates were cultured from the Wistar-Kyoto rat aorta. One group of cells, derived from early passages (3-5), proliferated with a cell doubling time of 2.41 days. A second group of cells, derived from late passages (> 12), proliferated at a higher rate (cell doubling time, 0.61 days). 3. Exposure of the early passaged cells to endothelin-1 (0.1 mumol/L) induced membrane depolarization. In contrast, exposure of the late passage cells to endothelin-1 (0.1 mumol/L) evoked a rapid hyperpolarization. The hyperpolarization in the late passage cells was blocked by charybdotoxin (20 nmol/L), an inhibitor of the large-conductance Calcium (Ca)-activated K+ channel. 4. The authors conclude that rapidly proliferating vascular smooth muscle cells express enhanced activity of Ca-activated K+ channels causing marked alterations in the electrical properties of the cells. It is therefore suggested that the reported increase in Ca-activated K+ channel activity in the aortae of hypertensive rats is likely to be associated with the increased proliferative ability of the vascular smooth muscle cells.

Animals↗
PubMed1994

Effect of transforming growth factor-beta 1 on platelet-derived growth factor receptor binding and gene expression in vascular smooth muscle cells from SHR and WKY rats.

1. This study examined the effects of transforming growth factor-beta 1 (TGF-beta 1) on platelet-derived growth factor-BB (PDGF-BB)-stimulated DNA synthesis, [125I]-PDGF-BB receptor binding and PDGF-beta receptor mRNA expression in vascular smooth muscle cells (VSMC) isolated from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). 2. TGF-beta 1 inhibited by 40% DNA synthesis stimulated by PDGF-BB in VSMC from WKY rats but potentiated by 20% growth factor-stimulated DNA synthesis in VSMC from the SHR. 3. Since the difference in effect of TGF-beta 1 could not be attributed to differential regulation of [125I]-PDGF-BB binding activity and PDGF-beta receptor mRNA expression, it is suggested that alterations in intracellular signalling pathways may account for the differential effects of TGF-beta 1 on PDGF-BB-stimulated DNA synthesis in VSMC from SHR and WKY rats.

Animals↗
PubMed1994

Developmentally regulated transforming growth factor-beta 1 action on vascular smooth muscle growth in the SHR.

1. This study examined the effects of transforming growth factor-beta 1 (TGF-beta 1) on platelet-derived growth factor-BB (PDGF-BB)-stimulated proliferation of vascular smooth muscle cells (VSMC) isolated from aortic tissue of 1, 4 and 12 week old spontaneously hypertensive rats (SHR). 2. In 1 week old SHR, TGF-beta 1 inhibited by about 60% VSMC proliferation stimulated by PDGF-BB; this inhibitory action of TGF-beta 1 was absent in VSMC isolated from 4 week old, prehypertensive SHR. In contrast, TGF-beta 1 potentiated by about 125% the mitogenic activity of PDGF-BB in VSMC cultures from adult SHR. 3. Age-dependent alterations in the action of TGF-beta 1 suggests an important role for TGF-beta 1 in the development of vascular hypertrophy from adolescence onwards in the SHR.

Animals↗
PubMed1994

Transforming growth factor-beta 1 gene activation and growth of smooth muscle from hypertensive rats.

Cultured vascular smooth muscle cells derived from the spontaneously hypertensive rat (SHR) are known to replicate more rapidly than cells from the normotensive Wistar-Kyoto (WKY) rat. In this study we compared the responses of vascular smooth muscle cells from the two strains to transforming growth factor-beta 1 (TGF-beta 1) and evaluated its potential to account for the different growth properties of these cells in response to a number of vascular-derived growth factors. TGF-beta 1 potentiated the proliferative effects of epidermal growth factor, basic fibroblast growth factor, or the different isoforms of platelet-derived growth factor on vascular smooth muscle cells from SHR but inhibited growth factor-stimulated proliferation of vascular smooth muscle cells from WKY rats. These differential effects of TGF-beta 1 on proliferation could not be attributed to alterations in the expression of the type I, II, or III TGF-beta receptors but appeared more related to the ability of cells to autoinduce the TGF-beta 1 gene. TGF-beta 1 caused a time-dependent increase in its own mRNA levels in vascular smooth muscle cells of WKY rats but attenuated levels in vascular smooth muscle cells of SHR. This effect was specific to TGF-beta 1 autoinduction since similar elevations in TGF-beta 1 mRNA levels were observed when vascular smooth muscle cells from the two rat strains were exposed to phorbol myristate acetate, basic fibroblast growth factor, or platelet-derived growth factor-BB.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Vascular hypertrophy in renal hypertensive spontaneously hypertensive rats.

Vascular smooth muscle cells isolated from spontaneously hypertensive rats (SHR) replicate faster in vitro than do cells from Wistar-Kyoto (WKY) rats, suggesting that the vascular hypertrophy seen early in the life of SHR might be at least partially caused by abnormal cellular growth properties in vivo. To test whether specific growth stimuli produce more extensive hypertrophy in SHR than WKY rats, we compared their cardiovascular growth responses to two-kidney, one clip renal hypertension. Six-week-old animals were subjected to either renal artery clipping or sham operation. Four weeks after renal artery clipping, there was a proportionately smaller rise in systolic blood pressure in SHR than WKY rats (21% and 44%, respectively); however, the overall level of systolic blood pressure achieved in the two rat strains differed by less than 10 mm Hg (4%). Limitations in the blood pressure responses of SHR to renal artery clipping were not due to inadequate development of left ventricular hypertrophy, as this was greater in SHR than WKY rats; however, aortic hypertrophy was similar in both strains. Aortic DNA content changes in SHR were consistent with a significant hyperplasia of medial smooth muscle cells, whereas in WKY rats, there was cellular hypertrophy. Small and medium-sized arteries of the mesenteric vasculature were also hypertrophied in SHR, and the medial cross-sectional area increased by 63% and 114%, respectively, compared with increases of only 15% and 23% in WKY rats. Strain differences between the sham-operated rat groups were small.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Different electrical responses to vasoactive agonists in morphologically distinct smooth muscle cell types.

Vascular smooth muscle cells (SMCs) in the blood vessel wall are frequently heterogeneous in nature, differing in their gross morphology, size, and shape, subcellular organelles, cytoskeleton, and contractile protein composition. In adult rat arterial vessels, two populations of SMCs have been shown to predominate: elongated bipolar cells, representing the majority of cells, and epithelial-like SMCs. We examined the ionic responses of these two types of SMCs, isolated by multiple subculture, to vasoactive stimuli. Elevations in intracellular Na+ and Ca2+ were measured with SBFI and fura 2, respectively, and changes in membrane potential were measured using the potential-sensitive fluorescent probe bis-oxonol. The resting membrane potential of the elongated bipolar cells was less negative than that of the epithelial-like SMCs. Exposure of the elongated SMCs to endothelin 1, alpha-thrombin, or arginine vasopressin induced elevations in [Ca2+]i and [Na+]i and membrane depolarization. Depolarization occurred because of entry of both Na+ and Ca2+, and pharmacological blockade of Cl- or K+ channels did not attenuate the depolarization. In contrast, when [Ca2+]i was elevated by the same agonists in the epithelial-like SMCs there was a pronounced hyperpolarization that appeared to be the consequence of enhanced activity of charybdotoxin-sensitive Ca(2+)-activated K+ channels because it was abolished by charybdotoxin (20 nmol/L), partially attenuated by tetraethylammonium chloride (10 mmol/L), and unaffected by apamin (1 mumol/L), glibenclamide (1 mumol/L), or 4-aminopyridine (5 mmol/L). Chelation of [Ca2+]i also abolished the hyperpolarization; instead, a small depolarization was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Cardiovascular hypertrophy in one-kidney, one clip renal hypertensive rats: a role for angiotensin II?

OBJECTIVE: To investigate the role of angiotensin II (Ang II) in cardiovascular hypertrophy in the Goldblatt one-kidney, one clip (1-K, 1C) renal hypertensive rat. METHODS: Six-week-old Wistar-Kyoto (WKY) rats underwent uninephrectomy and left renal artery clipping. After surgery, rats were treated with perindopril, an angiotensin converting enzyme (ACE) inhibitor, or losartan, an Ang II type 1 (AT1) receptor antagonist, for 4 weeks. Untreated 1-K, 1C rats and uninephrectomized (sham) rats served as controls. RESULTS: The rise in systolic blood pressure in the perindopril-treated and losartan-treated rats was not significantly different from that in the untreated 1-K, 1C group throughout the treatment period. At 4 weeks after surgery the heart weight:body weight ratios of the untreated 1-K, 1C and losartan-treated 1-K, 1C groups were significantly greater than for sham-operated normotensive rats and hypertensive perindopril-treated rats. The total number of smooth muscle cells in the thoracic aortae of the 1-K, 1C untreated, losartan-treated 1-K, 1C and sham groups were similar. However, after treatment the aortae of the perindopril-treated group contained significantly fewer smooth muscle cells. The medial cross-sectional wall area and wall: lumen ratio were similar in the 1-K, 1C untreated and perindopril-treated 1-K, 1C groups. CONCLUSION: These results suggest that Ang II, via its effects on cardiac and vascular AT1 receptors, does not contribute to the development of cardiovascular hypertrophy in the 1-K, 1C rat. Attenuation of cardiac and vascular growth after ACE inhibition appears to be mediated by mechanisms independent of the actions of the renin-angiotensin system.

Angiotensin II↗