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A study was conducted to analyze the influence of chronic angiotensin converting enzyme deficiency on the magnitude of tubuloglomerular feedback responses. The genotype was determined by polymerase chain reaction on DNA obtained from the tail. Results indicated that angiotensin II is an important component in the signal transmission pathway that connects the macula densa with the glomerular vascular pole.

The effect of the adenosine type 1 receptor agonist N(super 6)-cyclohexyladenosine (CHA) on glomerular vascular reactivity in angiotensin II type 1A receptor-deficient mice was investigated. Experimental results showed the inhibition of adenosine-1 receptor-mediated preglomerular vasoconstriction in male angiotensin II type 1A receptor knockout mice. It was also found that the decrease in stop-flow pressure after local administration of CHA is significantly affected in the receptor-deficient mice.

An analysis of the absence of the tobuloglomerular feedback (TGF) responses in AT1A receptor-deficient mice was presented. The study utilized TGF responses in a strain of mice that carries a null mutation in the angiotensin II AT1A receptor gene. Results of the analysis revealed that AT1A receptor-mediated effects of angiotensin II are significant components of TGF responsiveness.

A study of neuroregulation of electrolyte transport in the porcine distal colon using electrical transmural stimulation (ETS) shows that cholinergic submucosal neurons regulate epithelial ion transport in the porcine distal colon and neuropeptide Y(NPY) inhibits neural activity of leukotriene-sensitive neurons in the colon. ETS of the colonic mucosa submucosa incubated on Ussing chamber enhances short-circuit current indicating that part of response is mediated by Cl secretion.

Lorenz, John N., Patrick J. Schultheis, Timothy Traynor, Gary E. Shull, and Jurgen Schnermann. Micropuncture analysis of single-nephron function in NHE3-deficient mice. Am. J. Physiol. 277 (Renal Physiol. 46): F447-F453, 1999.--The Na/H exchanger isoform 3 (NHE3) is expressed in the proximal tubule and thick ascending limb and contributes to the reabsorption of fluid and electrolytes in these segments. The contribution of NHE3 to fluid reabsorption was assessed by micropuncture in homozygous ([Nhe3.sup.-/-]) and heterozygous ([Nhe3.sub.+/-]) knockout mice, and in their wild-type (WT, [Nhe3.sup.+/+]) littermates. Arterial pressure was lower in the [Nhe3.sup.-/-] mice (89 [+ or -] 6 mmHg) compared with [Nhe3.sup.+/+] (118 [+ or -] 4) and [Nhe3.sup.+/-] (108 [+ or -] 5). Collections from proximal and distal tubules demonstrated that proximal fluid reabsorption was blunted in both [Nhe3.sup.+/-] and [Nhe3.sup.-/-] mice (WT, 4.2 [+ or -] 0.3; [Nhe3.sup.+/-], 3.4 [+ or -] 0.2; and [Nhe3.sup.-/-], 2.6 [+ or -] 0.3 nl/min; P [is less than] 0.05). However, distal delivery of fluid was not different among the three groups of mice (WT, 3.3 [+ or -] 0.4 nl/min; [Nhe3.sup.+/-], 3.3 [+ or -] 0.2 nl/min; and [Nhe3.sup.-/-], 3.0 [+ or -] 0.4 nl/min; P [is less than] 0.05). In [Nhe3.sup.-/-] mice, this compensation was largely attributable to decreased single-nephron glomerular filtration rate (SNGFR): 10.7 [+ or -] 0.9 nl/min in the [Nhe3.sup.+/+] vs. 6.6 [+ or -] 0.8 nl/min in the [Nhe3.sup.-/-], measured distally. Proximal-distal SNGFR differences in [Nhe3.sup.-/-] mice indicated that much of the decrease in SNGFR was due to activation of tubuloglomerular feedback (TGF), and measurements of stop-flow pressure confirmed that TGF is intact in [Nhe3.sup.-/-] animals. In contrast to [Nhe3.sup.-/-] mice, normalization of early distal flow rate in [Nhe3.sup.+/-] mice was not related to decreased SNGFR (9.9 [+ or -] 0.7 nl/min), but rather, to increased fluid reabsorption in the loop segment ([Nhe3.sup.+/+], 2.6 [+ or -] 0.2; [Nhe3.sup.+/-], 3.6 [+ or -] 0.5 nl/min). We conclude that NHE3 is a major Na/H exchanger isoform mediating [Na.sup.+] and fluid reabsorption in the proximal tubule. In animals with NHE3 deficiency, normalization of fluid delivery to the distal tubule is achieved through alterations in filtration rate and/or downstream transport processes. kidney; single-nephron glomerular filtration rate; sodium/ proton exchange; proximal tubule; tubuloglomerular feed-back

Examines which cyclooxygenase (COX) isoform is involved in sodium chloride (NaCl)-dependent renin secretion. Renin content of each superfusate sample; Effect of valerylsalicylate on renin secretion; How changes in luminal NaCl concentration affect macula densa prostaglandin production.

Assesses tubuloglomerular feedback responses in mice that carries a null mutation in the angiotensin II AT1A receptor gene. Dose-response relationship between mean arterial blood pressure and single bolus injections of angiotensin II; Feasibility of utilizing complex micropuncture approaches to assess glomerular and tubular function in genetically altered mice.