Effect of adrenergic agonists on big and small renin

Itoh, Hiroshi; Lin, Cherry; Michelakis, Andrew M.

doi:10.1152/ajpendo.1980.238.5.e416

Cited by 6 publications

(5 citation statements)

References 17 publications

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“…The elution characteristics of the various forms of renin from plasma of nontreated mice has been reported previously ( 12). semide (control group), the plasma level of big renin was higher than that of small renin.…”

Section: Measurement Of Reninsupporting

confidence: 52%

“…Acute stimulation of renin release by furosemide, isoproterenol, tilting, or diazoxide increased active or small renin in human (20, 24), pig (21), dog (18), and mouse (12). Inactive or big renin was not changed in dog by furosemide (18), slightly increased in human by furosemide and isoproterenol (20,24), and greatly increased in pig by furosemide and isoproterenol (21), and in mouse by isoproterenol (12).…”

Section: Measurement Of Reninmentioning

confidence: 98%

“…The high-molecular-weight renins are considered to be renins because they were enzymatically active by generating angiotensin I, and their enzymatic activity was neutralized by renin antibody and pepstatin (12). The column was equilibrated and eluted with 0.05 M sodium phosphate buffer, pH 7.4, containing 0.1 M sodium chloride and 0.02% sodium azide at a rate of 0.625 mVhr.…”

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confidence: 99%

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Effect of Furosemide and Dietary Sodium on Kidney and Plasma Big and Small Renin

Itoh

Michelakis

1981

Experimental Biology and Medicine

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Renin was found in mouse plasma in high-molecular-weight forms (big big renin, big renin) and a low-molecular-weight form (small renin). They were measured by a radioimmunoassay procedure for the direct measurement of renin. In the kidney, 89% of total renin was small renin and the rest was big big and big renin. This distribution pattern of renins was not changed when the kidney tissue was homogenized in the presence of protease inhibitors. Low-sodium or high-sodium diets changed renal renin content, but not the distribution pattern of renins in the kidney. Acute stimulation of renin release by furosemide increased small renin but not big big and big renin in plasma. However, dietary sodium depletion for 2 weeks significantly increased big big, big, and small renin in plasma of mice with or without submaxillary glands. In contrast, high-sodium intake significantly decreased big big, big, and small renin in plasma of mice with or without submaxillary glands. 36 1 0037-972718 11 1 10361-08$0 1 .OO/O

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Section: Measurement Of Reninsupporting

confidence: 52%

Section: Measurement Of Reninmentioning

confidence: 98%

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confidence: 99%

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Effect of Furosemide and Dietary Sodium on Kidney and Plasma Big and Small Renin

Itoh

Michelakis

1981

Experimental Biology and Medicine

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“…This is consistent with the findings of earlier studies that reported values of 30% to 50%. 29,30 Although Poulsen and coworkers reported a value of 80% to 90% prorenin for male mice, 31 they commented that the proportion of prorenin measured in the plasma of female mice was around 50%. 32 In the present study, mouse prorenin levels were similarly higher in male than female mice on a normal salt diet, but these differences disappeared in the responses to dietary salt or captopril; none of the differences were significant, possibly due to the small number of males that were tested (9 of 36).…”

Section: Discussionmentioning

confidence: 99%

Appropriate Regulation of Human Renin Gene Expression and Secretion in 45-kb Human Renin Transgenic Mice

Yan

Chen

et al. 1998

Hypertension

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Abstract-To create physiological models of the human renin-angiotensin system in transgenic animals, the component genes should be expressed in the correct tissues and cells and respond appropriately to physiological stimuli. We recently showed that mice carrying a 45-kb human renin genomic fragment, containing approximately 25 kb 5Ј-flanking DNA and 6 kb 3Ј-flanking DNA, express the transgene in a highly cell-and tissue-specific pattern. More importantly, in contrast to previous models, human renin in the circulating plasma of these mice is derived exclusively from the kidneys. In the present study, we tested the responses of both human and mouse renal renin expression and secretion of the 45-kb hREN transgenic mice to a variety of physiological and pharmacological stimuli. A sodium-deficient diet, angiotensin-converting enzyme inhibition, and ␤ 1 -adrenergic stimulation each increased both human and mouse plasma renin concentration significantly, whereas elevated blood pressure and/or increased plasma angiotensin II levels suppressed them. Human and mouse renal renin mRNA levels changed similarly but to a lesser degree. These studies demonstrate that human renin synthesis and secretion respond appropriately in 45-kb hREN mice to physiological stimuli. This most likely results from appropriate cell-specific expression of the transgene conferred by the extended transgene flanking sequences. (Hypertension. 1998;32:205-214.)

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“…per pg renin, of renin in isoproterenoland phenylephrine-saliva were 0.58 and 0.45 G.U./[i.g, respec¬ tively. Therefore the high molecular weight forms of renin found in plasma from nephrectomized mice (Mailing & Poulsen 1977b;Iwao et al 1980) are probably not secretory pro¬ ducts from the submaxillary gland. /[ig (Pedersen & Poulsen 1981).…”

Section: Discussionmentioning

confidence: 99%

Vast release of submaxillary mouse renin to saliva after stimulation with cholinergic, β-adrenergic but especially α-adrenergic agonists

Pedersen

Poulsen

1982

Acta Endocrinologica

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\g=a\-adrenergic stimulation with phenylephrine causes release of vast amounts of mouse submaxillary gland renin to saliva. The amount released is about 100-fold higher than that released after \g=b\-adrenergic stimulation with isoproterenol and about 1000-fold higher than the amount released after cholinergic stimulation with pilocarpine. \g=a\-blockadewith phenoxybenzamine before phenylephrine stimulation strongly inhibits the renin release. However, phenoxybenzamine or \ g = b \ \ x = r e q -\ blockade with propranolol before isoproterenol stimulation have no effect on the amount of renin released.Thus, the release of submaxillary mouse renin to saliva is triggered mainly by activation of \g=a\-adrenergicreceptors. Renin in cholinergic and \g=a\-and \g=b\-adrenergic stimulated saliva has the same molecular weight and the same specific enzymatic activity as renin in the submaxillary gland. This indicates that renin is secreted to saliva, and probably also to the blood, in its fully enzymically active 40000 mol. wt. form regardless of the stimulus used. The vast amounts of renin released to saliva (up to 600 Goldblatt Units) demonstrate that submaxillary mouse renin is secreted predominantly to saliva and much less to the blood. The mouse submaxillary gland therefore seems to have an exocrine rather than an endocrine role for release of renin.

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Effect of adrenergic agonists on big and small renin

Cited by 6 publications

References 17 publications

Effect of Furosemide and Dietary Sodium on Kidney and Plasma Big and Small Renin

Effect of Furosemide and Dietary Sodium on Kidney and Plasma Big and Small Renin

Appropriate Regulation of Human Renin Gene Expression and Secretion in 45-kb Human Renin Transgenic Mice

Vast release of submaxillary mouse renin to saliva after stimulation with cholinergic, β-adrenergic but especially α-adrenergic agonists

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