Recruited renin-containing renal microvascular cells demonstrate the calcium paradox regulatory phenotype
Spencer MacGriff,1 Richard E Woo,1 M Cecilia Ortiz-Capisano,1 Douglas K Atchison,1,2 William H Beierwaltes1,2 1Department of Internal Medicine, Hypertension and Vascular Research Division, Henry Ford Hospital, 2Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA Ab...
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| Format: | Article |
| Language: | English |
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Dove Medical Press
2014-01-01
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| Series: | Integrated Blood Pressure Control |
| Online Access: | http://www.dovepress.com/recruited-renin-containing-renal-microvascular-cells-demonstrate-the-c-a15495 |
| _version_ | 1811252510588928000 |
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| author | MacGriff S Woo RE Ortiz-Capisano MC Atchison DK Beierwaltes WH |
| author_facet | MacGriff S Woo RE Ortiz-Capisano MC Atchison DK Beierwaltes WH |
| author_sort | MacGriff S |
| collection | DOAJ |
| description | Spencer MacGriff,1 Richard E Woo,1 M Cecilia Ortiz-Capisano,1 Douglas K Atchison,1,2 William H Beierwaltes1,2 1Department of Internal Medicine, Hypertension and Vascular Research Division, Henry Ford Hospital, 2Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA Abstract: Renin is the critical regulatory enzyme for production of angiotensin (Ang)-II, a potent vasoconstrictor involved in regulating blood pressure and in the pathogenesis of hypertension. Chronic sodium deprivation enhances renin secretion from the kidney, due to recruitment of additional cells from the afferent renal microvasculature to become renin-producing rather than just increasing release from existing juxtaglomerular (JG) cells. JG cells secrete renin inversely proportional to extra- and intracellular calcium, a unique phenomenon characteristic of the JG regulatory phenotype known as the “calcium paradox.” It is not known if renin secreted from recruited renin-containing cells is regulated similarly to native JG cells, and therefore acquires this JG cell phenotype. We hypothesized that non-JG cells in renal microvessels recruited to produce renin in response to chronic dietary sodium restriction would demonstrate the calcium paradox, characteristic of the JG cell phenotype. Histology showed recruitment of upstream arteriolar renin in response to sodium restriction compared to normal-diet rats. Renin fluorescence intensity increased 53% in cortices of sodium-restricted rats (P<0.001). We measured renin release from rat afferent microvessels, isolated using iron oxide nanopowder and incubated in either normal or low-calcium media. Basal renin release from normal sodium-diet rat microvessels in normal calcium media was 298.1±44.6 ng AngI/mL/hour/mg protein, and in low-calcium media increased 39% to 415.9±71.4 ng AngI/mL/hour/mg protein (P<0.025). Renin released from sodium-restricted rat microvessels increased 50% compared to samples from normal-diet rats (P<0.04). Renin release in normal calcium media was 447.0±54.3 ng AngI/mL/hour/mg protein, and in low-calcium media increased 36% to 607.6±96.1 ng AngI/mL/hour/mg protein (P<0.05). Thus, renin-containing cells recruited in the afferent microvasculature not only express and secrete renin but demonstrate the calcium paradox, suggesting renin secretion from recruited renin-containing cells share the JG phenotype for regulating renin secretion. Keywords: renin recruitment, calcium, renal microvessels, prorenin, low-salt diet, afferent arteriole |
| first_indexed | 2024-04-12T16:35:41Z |
| format | Article |
| id | doaj.art-7716d00998294f57bddad735190002c8 |
| institution | Directory Open Access Journal |
| issn | 1178-7104 |
| language | English |
| last_indexed | 2024-04-12T16:35:41Z |
| publishDate | 2014-01-01 |
| publisher | Dove Medical Press |
| record_format | Article |
| series | Integrated Blood Pressure Control |
| spelling | doaj.art-7716d00998294f57bddad735190002c82022-12-22T03:24:59ZengDove Medical PressIntegrated Blood Pressure Control1178-71042014-01-012014default91715495Recruited renin-containing renal microvascular cells demonstrate the calcium paradox regulatory phenotypeMacGriff SWoo REOrtiz-Capisano MCAtchison DKBeierwaltes WHSpencer MacGriff,1 Richard E Woo,1 M Cecilia Ortiz-Capisano,1 Douglas K Atchison,1,2 William H Beierwaltes1,2 1Department of Internal Medicine, Hypertension and Vascular Research Division, Henry Ford Hospital, 2Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA Abstract: Renin is the critical regulatory enzyme for production of angiotensin (Ang)-II, a potent vasoconstrictor involved in regulating blood pressure and in the pathogenesis of hypertension. Chronic sodium deprivation enhances renin secretion from the kidney, due to recruitment of additional cells from the afferent renal microvasculature to become renin-producing rather than just increasing release from existing juxtaglomerular (JG) cells. JG cells secrete renin inversely proportional to extra- and intracellular calcium, a unique phenomenon characteristic of the JG regulatory phenotype known as the “calcium paradox.” It is not known if renin secreted from recruited renin-containing cells is regulated similarly to native JG cells, and therefore acquires this JG cell phenotype. We hypothesized that non-JG cells in renal microvessels recruited to produce renin in response to chronic dietary sodium restriction would demonstrate the calcium paradox, characteristic of the JG cell phenotype. Histology showed recruitment of upstream arteriolar renin in response to sodium restriction compared to normal-diet rats. Renin fluorescence intensity increased 53% in cortices of sodium-restricted rats (P<0.001). We measured renin release from rat afferent microvessels, isolated using iron oxide nanopowder and incubated in either normal or low-calcium media. Basal renin release from normal sodium-diet rat microvessels in normal calcium media was 298.1±44.6 ng AngI/mL/hour/mg protein, and in low-calcium media increased 39% to 415.9±71.4 ng AngI/mL/hour/mg protein (P<0.025). Renin released from sodium-restricted rat microvessels increased 50% compared to samples from normal-diet rats (P<0.04). Renin release in normal calcium media was 447.0±54.3 ng AngI/mL/hour/mg protein, and in low-calcium media increased 36% to 607.6±96.1 ng AngI/mL/hour/mg protein (P<0.05). Thus, renin-containing cells recruited in the afferent microvasculature not only express and secrete renin but demonstrate the calcium paradox, suggesting renin secretion from recruited renin-containing cells share the JG phenotype for regulating renin secretion. Keywords: renin recruitment, calcium, renal microvessels, prorenin, low-salt diet, afferent arteriolehttp://www.dovepress.com/recruited-renin-containing-renal-microvascular-cells-demonstrate-the-c-a15495 |
| spellingShingle | MacGriff S Woo RE Ortiz-Capisano MC Atchison DK Beierwaltes WH Recruited renin-containing renal microvascular cells demonstrate the calcium paradox regulatory phenotype Integrated Blood Pressure Control |
| title | Recruited renin-containing renal microvascular cells demonstrate the calcium paradox regulatory phenotype |
| title_full | Recruited renin-containing renal microvascular cells demonstrate the calcium paradox regulatory phenotype |
| title_fullStr | Recruited renin-containing renal microvascular cells demonstrate the calcium paradox regulatory phenotype |
| title_full_unstemmed | Recruited renin-containing renal microvascular cells demonstrate the calcium paradox regulatory phenotype |
| title_short | Recruited renin-containing renal microvascular cells demonstrate the calcium paradox regulatory phenotype |
| title_sort | recruited renin containing renal microvascular cells demonstrate the calcium paradox regulatory phenotype |
| url | http://www.dovepress.com/recruited-renin-containing-renal-microvascular-cells-demonstrate-the-c-a15495 |
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