{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T23:43:27Z","timestamp":1784245407164,"version":"3.55.0"},"reference-count":42,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/501100000850","name":"National Heart and Lung Institute (NHLI)","doi-asserted-by":"publisher","award":["HL-028982"],"award-info":[{"award-number":["HL-028982"]}],"id":[{"id":"10.13039\/501100000850","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,12,1]]},"abstract":"<jats:p> Zucker obese rats (ZOR) have higher glomerular capillary pressure (P<jats:sub>GC<\/jats:sub>) that can cause renal damage. P<jats:sub>GC<\/jats:sub> is controlled by afferent (Af-Art) and efferent arteriole (Ef-Art) resistance. Af-Art resistance is regulated by factors that regulate other arterioles, such as myogenic response. In addition, it is also regulated by 2 intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the connecting tubule via the epithelial sodium channel. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that increased CTGF contributes to TGF attenuation, which in turn increases P<jats:sub>GC<\/jats:sub> in ZOR. We performed a renal micropuncture experiment and measured stop-flow pressure (P<jats:sub>SF<\/jats:sub>), which is an indirect measurement of P<jats:sub>GC<\/jats:sub> in ZOR. Maximal TGF response at 40 nl\/min was attenuated in ZOR (4.47\u2009\u00b1\u20090.60 mmHg) in comparison to the Zucker lean rats (ZLR; 8.54\u2009\u00b1\u20090.73 mmHg, P &lt; 0.05), and CTGF was elevated in ZOR (5.34\u2009\u00b1\u20090.87 mmHg) compared with ZLR (1.12\u2009\u00b1\u20091.28 mmHg, P &lt; 0.05). CTGF inhibition with epithelial sodium channel blocker normalized the maximum P<jats:sub>SF<\/jats:sub> change in ZOR indicating that CTGF plays a significant role in TGF attenuation (ZOR, 10.67\u2009\u00b1\u20091.07 mmHg vs. ZLR, 9.5\u2009\u00b1\u20091.53 mmHg). We conclude that enhanced CTGF contributes to TGF attenuation in ZOR and potentially contribute to progressive renal damage. <\/jats:p>","DOI":"10.1152\/ajprenal.00227.2018","type":"journal-article","created":{"date-parts":[[2018,10,10]],"date-time":"2018-10-10T13:31:11Z","timestamp":1539178271000},"page":"F1708-F1713","source":"Crossref","is-referenced-by-count":8,"title":["Role of connecting tubule glomerular feedback in obesity related renal damage"],"prefix":"10.1152","volume":"315","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1906-3063","authenticated-orcid":false,"given":"Sumit R.","family":"Monu","sequence":"first","affiliation":[{"name":"Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mani","family":"Maheshwari","sequence":"additional","affiliation":[{"name":"Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan"},{"name":"Department of Pharmacology, Physiology and Toxicology, Joan C. 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