The overall aim of this proposal is to advance our understanding of the urinary concentrating mechanism by exploiting the knowledge obtained from the unique avian kidney model. Birds and mammals are the only vertebrates that can produce urine hyperosmotic to plasma, but structure and function of the countercurrent system for urine concentration appear to be different. In bird kidneys: 1) superficial reptilian-type (RT) and medullary mammalian-type (MT) nephrons exist; 2) an inner medulla and papilla are absent; 3) NaCl but not urea composes a corticomedullary osmotic gradient; and 4) hyposmotic drainage from RT nephrons alters urine flow and concentration. Based on these features, we propose to conduct two projects using the in vitro perfused tubule from the quail, Coturnix coturnix. Project I is to determine whether a simpler counter-current multiplication model based on NaCl transport operates between the TAL and the descending limb (DL) of the MT nephron. We will measure in the DL diffusional potentials, and permeabilities and fluxes for Na, Cl, and water. Na-K-ATPase activity of nephrons and architectural organization of the medulla will be examined. Project II aims to determine whether reductions in the volume flow rate through the collecting duct would improve urine concentrating ability in the absence of arginine vasotocin (AVT, avian antidiuretic hormone). We will measure, first, whether AVT increases osmotic water permeability and adenylate cyclase activity of the collecting duct and, second, whether a reduction of the perfusion flow rate alters net fluid transport and osmotic water permeability in the absence of AVT. Definition of the operational characteristics of the avian urinary concentrating mechanism, as compared to those of the mammalian system, will: 1) aid in clarifying fundamental problems underlying the concentrating mechanism of the mammalian kidney, and 27 provide new insights concerning common features that were necessary to adapt the primitive vertebrate kidney to permit formation of concentrated urine.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
2R01HL029364-04A1
Application #
3340465
Study Section
Experimental Cardiovascular Sciences Study Section (ECS)
Project Start
1982-08-01
Project End
1989-03-31
Budget Start
1986-04-01
Budget End
1987-03-31
Support Year
4
Fiscal Year
1986
Total Cost
Indirect Cost
Name
University of Tennessee Health Science Center
Department
Type
Schools of Medicine
DUNS #
941884009
City
Memphis
State
TN
Country
United States
Zip Code
38163
Qin, Z L; Nishimura, H (1998) Ca2+ signaling in fowl aortic smooth muscle increases during maturation but is impaired in neointimal plaques. J Exp Biol 201:1695-705
Nishimura, H; Koseki, C; Patel, T B (1996) Water transport in collecting ducts of Japanese quail. Am J Physiol 271:R1535-43
Kamimura, K; Nishimura, H; Bailey, J R (1995) Blockade of beta-adrenoceptor in control of blood pressure in fowl. Am J Physiol 269:R914-22
Nishimura, H; Walker, O E; Patton, C M et al. (1994) Novel angiotensin receptor subtypes in fowl. Am J Physiol 267:R1174-81
Osono, E; Nishimura, H (1994) Control of sodium and chloride transport in the thick ascending limb in the avian nephron. Am J Physiol 267:R455-62
Hasegawa, K; Nishimura, H; Khosla, M C (1993) Angiotensin II-induced endothelium-dependent relaxation of fowl aorta. Am J Physiol 264:R903-11
Nakamura, Y; Madey, M A; Nishimura, H et al. (1992) Lack of control of renin release by adrenergic nervous system in the aglomerular toadfish. Gen Comp Endocrinol 88:62-75
Hasegawa, K; Nishimura, H (1991) Humoral factor mediates acetylcholine-induced endothelium-dependent relaxation of chicken aorta. Gen Comp Endocrinol 84:164-9
Stallone, J N; Nishimura, H; Nasjletti, A (1990) Angiotensin II binding sites in aortic endothelium of domestic fowl. Am J Physiol 258:R777-82
Nishimura, H; Koseki, C; Imai, M et al. (1989) Sodium chloride and water transport in the thin descending limb of Henle of the quail. Am J Physiol 257:F994-1002

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