Changes in renal .ALPHA.2-adrenoceptor in experimental hypertension in rats.

Fukuda, Kazuya; Kuchii, Masato; Hano, Takuzo; Mohara, Osamu; Miyamoto, Yasumasa; Nishio, Ichiro; Masuyama, Yoshiaki

doi:10.1253/jcj.47.1221

Cited by 16 publications

(4 citation statements)

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“…Although systolic blood pressure was higher in SHR than in WKY rats at all age groups in that study, this difference reached statistical significance only starting at 8 weeks with the given sample size. Fukuda et al 19 detected significantly elevated renal a 2 -adrenergic receptors in 4-week-old SHR but did not report blood pressure values for these animals. The present study failed to detect significant alterations of «]-or a 2 -adrenergic receptors in 3-week-old SHR.…”

Section: Fig 6 Line Graphs Show Development Of Basal and Isoproterenmentioning

confidence: 91%

“…1718 Elevations of both a r and a 2 -adrenergic receptor numbers have been reported to precede the development of hypertension. 19 ' 20 Based on these findings, we have previously hypothesized that genetically determined alterations of renal a-adrenergic receptors might play an important pathophysiological role in the development of hypertension in the SHR. 21 More recent studies in our laboraby guest on May 9, 2018 http://hyper.ahajournals.org/ Downloaded from tory, however, have argued against a role for genetically determined alterations for a 1A -, a 1B -, or a^-adrenergic receptor number in the development of hypertension in the SHR.…”

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confidence: 99%

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Ontogenesis of sympathetic responsiveness in spontaneously hypertensive rats. I. Renal alpha 1-, alpha 2-, and beta-adrenergic receptors and their signaling.

et al. 1993

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We studied the ontogenetic development of renal t v , o^-, and /3-adrenergic receptors and their coupling to inositol phosphate and cyclic AMP formation in spontaneously hypertensive and normotensive Wistar-Kyoto rats, a,-, <%-, and /3-Adrenergic receptor number was significantly increased in hypertensive compared with normotensive rats, but the increase did not precede blood pressure elevation. Despite increased a,-adrenergic receptors, basal and norepinephrine-stimulated inositol phosphate formation remained unchanged in all age groups. Rat kidney contains a, A -and «, B -adrenergic receptors coupling to inositol phosphate formation by different mechanisms, but the relative contribution of «, A -and ff, B -adrenergic receptors to norepinephrine-stimulated inositol phosphate formation was similar in normotensive and hypertensive rats. Despite increased /3-adrenergic receptors, basal, isoproterenol-, and forskolin-stimulated cyclic AMP accumulation was similar in normotensive and hypertensive rats. We conclude that the number but not the functional responsiveness of renal adrenergic receptors increases in spontaneously hypertensive rats. Thus, the additional receptors are unlikely to contribute to the pathophysiology of elevated blood pressure in this model.

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Section: Fig 6 Line Graphs Show Development Of Basal and Isoproterenmentioning

confidence: 91%

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confidence: 99%

Ontogenesis of sympathetic responsiveness in spontaneously hypertensive rats. I. Renal alpha 1-, alpha 2-, and beta-adrenergic receptors and their signaling.

et al. 1993

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“…In acquired forms of hypertension, renal x-adrenoceptor density has been found to be unchanged or decreased (Yamada et al, 1980;Fukuda et al, 1983;Saiz et al, 1987;Michel et al, 1989b;Wilson, 1991), whereas in spontaneously hypertensive rats, the density of renal a2-adrenoceptors has been found to be elevated as compared to Wistar-Kyoto rats (Pettinger et al, 1982;Saiz et al, 1987;Sanchez et al, 1989;Michel et al, 1990a). Furthermore, previous studies in our laboratory indicated that the renal response to M2-adrenoceptor agonists such as clonidine was decreased in spontaneously hypertensive rats (Li et al, 1992) but not in one kidney, one clip (1K-IC) hypertensive rats (Li & Smyth, 1994).…”

Section: Introductionmentioning

confidence: 99%

Attenuated renal response to moxonidine and rilmenidine in one kidney‐one clip hypertensive rats

Penner

Smyth

1994

British J Pharmacology

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1I, non-adrenoceptor, imidazoline receptor agonists, such as moxonidine, increase urine flow rate and sodium excretion following infusion into the renal artery. The functions of these agonists in genetic and acquired models of hypertension have not been determined. 2 We therefore studied the renal effects of two known non-adrenoceptor, imidazoline receptor agonists, rilmenidine and moxonidine, in 1K-IC hypertensive and 1K-sham normotensive rats. Rilmenidine (0, 3, 10, 30 nmol kg-' min-') or moxonidine (0, 1, 3, 10 nmol kg-' min-') was infused directly into the renal artery (30 gauge needle) of 1K-sham normotensive and 1K-IC hypertensive rats. 3 In 1K-sham normotensive rats, rilmenidine and moxonidine produced dose related increases in urine flow rate, sodium excretion and osmolar clearance. Both rilmenidine and moxonidine failed to increase urine flow rate, sodium excretion and osmolar clearance in 1K-IC hypertensive rats to the same extent as in 1K-sham animals. At comparable doses, rilmenidine had no effect, while moxonidine (3 and 10 nmol kg-' min-') did result in a small increase in urine volume and osmolar clearance which was less than that observed in the 1K sham control animals. 4 These studies indicate that the renal effects of non-adrenoceptor, imidazoline receptor stimulation are diminished in 1K-IC hypertensive rats compared with 1K-sham normotensive rats. Whether this decrease in activity of the natriuretic non-adrenoceptor, imidazoline receptors contributes to the increase in blood pressure in the 1K-IC acquired model of hypertension remains to be determined.

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“…Key Words: a2-adrenoceptor, SHR, RFLP A pathogenetic role of altered a2-adrenoceptors in essential hypertension has been suggested in both human and animal studies. Renal a2-adrenoceptor density is increased in genetically hypertensive rats and this increase precedes the development of highblood pressure and does not occur in animal models of acquired hypertension (1)(2)(3)(4)(5)(6)(7)(8) . High dietary sodium chloride augments both the blood pressure and the already increased renal a2-adrenoceptor density in most genetically hypertensive rats (7,9).…”

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Mapping of a Dde I RELP of the .ALPHA.2-Adrenoceptor Gene and the Correlation of Genotype with Blood Pressure in the F2 Rats of SHR-WKY Cross.

et al. 1992

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To examine a pathogenetic role of a2-adrenoceptor (a2-AR) in genetically hypertensive rats, we compared the a2-AR gene of spontaneously hypertensive rats (SHR) and its normotensive control Wistar-Kyoto (WKY) rats by restriction fragment length polymorphism (RFLP) analysis and did a genetic cosegregation study. After screening with 52 restriction endonucleases (RE), an RFLP was found by digestion of the genomic DNA of SHR and WKY rat with Dde I RE and using a human platelet a2-AR probe, the gene (ADRA2R) which is localized in chromosome 10. Restriction mapping analysis revealed that the RFLP is located in the 5' region of the a2-AR gene. This RFLP was used as a marker in a genetic cosegregation study to examine the correlation of genotype with blood pressure in F2 rats of SHR and WKY rat cross. The distribution of the genotypes based on the RFLP conformed to a 1:2:1 ratio in male F2 rats as expected for Mendelian inheritance, but not in female F2 rats. The number of female F2 rats with double SHR alleles was decreased about 68% from expected. Blood pressure of the male or female F2 rats homozygous for the SHR a2-adrenoceptor alleles was not significantly higher than the F2 rats heterozygous or homozygous for the WKY alleles with either indirect or direct blood pressure measurement.The additional finding was that males had higher blood pressure than females. This study ruled out the cosegregation of a2-adrenoceptor RFLP with higher blood pressure in the F2 rats of SHR and WKY cross. However, Since the abnormality of the renal a2-adrenoceptor in genetically hypertensive rats is one of altered regulation, and the RFLP we found is located in the 5' region of the gene where functionally important sequences are located which regulate gene expression, this RFLP may still be of interest in genetically hypertensive rats. (Hypertens Res 1992; 15: 143-148) A pathogenetic role of altered a2-adrenoceptors in essential hypertension has been suggested in both human and animal studies. Renal a2-adrenoceptor density is increased in genetically hypertensive rats and this increase precedes the development of highblood pressure and does not occur in animal models of acquired hypertension (1-8) . High dietary sodium chloride augments both the blood pressure and the already increased renal a2-adrenoceptor density in most genetically hypertensive rats (7, 9). A genetically determined increase in renal a2-adrenoceptor density could raise renal vascular resistance, increase Na and water reabsorption and play a role in the pathogenesis of genetic hypertension (10-I1). Cerebral a2-adrenoceptors are also increased in spontaneously hypertensive rats (SHR)(12) but not in deoxycorticosterone acetate salt hypertensive rats (8).In humans, Brodde et al. (13) found increased platelet a2-adrenoceptor density in 40 male hypertensive patients compared to normotensive patients. Moreover, the aggregation of platelets in response to 10 pM epinephrine (acting via a2-adrenoceptors) was enhanced in the hypertensive patients suggesting functional signif...

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Changes in renal .ALPHA.2-adrenoceptor in experimental hypertension in rats.

Cited by 16 publications

References 10 publications

Ontogenesis of sympathetic responsiveness in spontaneously hypertensive rats. I. Renal alpha 1-, alpha 2-, and beta-adrenergic receptors and their signaling.

Ontogenesis of sympathetic responsiveness in spontaneously hypertensive rats. I. Renal alpha 1-, alpha 2-, and beta-adrenergic receptors and their signaling.

Attenuated renal response to moxonidine and rilmenidine in one kidney‐one clip hypertensive rats

Mapping of a Dde I RELP of the .ALPHA.2-Adrenoceptor Gene and the Correlation of Genotype with Blood Pressure in the F2 Rats of SHR-WKY Cross.

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