The views expressed in this commentary are solely the responsibility of the authors and they do not necessarily reflect the views, decisions, or policies of the institutions with which they are affiliated.

Although the presence of granulomas can support a diagnosis of Crohn disease, severe inflammation and other abnormalities occur in the proximal gastrointestinal tract in Crohn disease and ulcerative colitis.

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ThedaytimefastingofRamadanisobservedannuallyby millions of adult Muslims all over the world. Some may have mild, moderate or severe medical conditions. They may seek advice on feasibility and safety of fasting and/ ortheirmanagement.Physiciansoughttohaveaworking knowledgeaboutthereligiousrulesofRamadanfastand theirmedicalimplications.Inthisarticlewepresentaconcise summaryoftheproceedingsofaseriesofsymposia.Their objectivesweretoreviewtheeffectsofRamadanfastingon thehealthofMuslimpatientswithvariouschronicmedical conditionsandtoproposepracticalmanagementstrategies. An initial introductory Islamic perspective on fasting to setthesceneforthefollowingpresentations.Thereligious rulingsexcludingpatientswithacuteandchronicmedical conditionsfromfastingwerehighlighted.Therolesofthe medicalprofessionalinguidingpatientsonbestwaystomake

Acid-base status and renal acid excretion were studied in the Dahl/Rapp salt-sensitive (S) rat and its genetically salt-resistant counterpart (R). S rats developed hypertension while on a very high salt diet (8%) and while on a more physiological salt diet (1%) and remained normotensive while on a very low salt diet (0.08%). Under the high salt diet, intracellular pH measured in freshly isolated thymic lymphocytes using 2',7'-bis (carboxyethyl)-5 (6)-carboxyfluorescein acetomethyl ester, a pH-sensitive dye, was lower in S than in R rats both when measured in the presence of HCO3/CO2 (7.32±0.02 vs. 7.38±0.02, respectively, P < 0.05) and in its absence (7.18±0.04 vs. 7.27±0.02, respectively, P < 0.05). Under the high salt diet, net acid excretion was higher in S than R rats (1,777±111 vs. 1,017±73 gEq/24 h per 100 g body wt, respectively, P < 0.001), and this difference was due to higher rates of both titratable acid and ammonium excretion. Directionally similar differences in intracellular pH and net acid excretion between S and R rats were also observed in salt-restricted animals. In S and R rats placed on a normal salt intake (1%) and strictly pair-fed to control food intake as a determinant of dietary acid, net acid excretion was also higher in S than in R rats (562±27 vs. 329±21 ,uEq/24 h per 100 g, respectively, P < 0.01). No significant difference in either blood pH or bicarbonate levels were found between S and R rats on either the 0.08%, 1%, or 8% salt diets. We conclude that renal acid excretion is augmented in the salt-sensitive Dahl/Rapp rat. Enhanced renal acid excretion may be a marker of increased acid production by cells from subjects with salt-sensitive hypertension. (J. Clin. Invest. 1993. 91:2178-2184 Key words: saltsensitive hypertension * acid excretion * intracellular pH -Na+ / H + antiporter * acid base

Enhanced activity of the Na+/H' antiporter is increasingly reported as a feature of cells from hypertensive subjects but the intracellular pH (ipH) dependency of its activity has not been examined. This study was designed to characterize the kinetic properties of the Na+/H' antiporter in lymphocytes from adult spontaneously hypertensive rats (SHR) and in those from age-matched normotensive Wistar-Kyoto (WKY) controls. Steady-state ipH, estimated from the measurement of BCECF fluorescence, was significantly lower in lymphocytes from the SHR than in those from WKY rats (7.09±0.02, n = 17 and 7.17±0.03, n = 19, respectively, P < 0.025). The velocity of the antiporter determined from the product of the We conclude that while the ipH of SHR lymphocytes is reduced, the kinetic properties of the Na+/H' antiporter are virtually identical in SHR and WKY lymphocytes. Consequently, a primary abnormality in the activity of this antiporter is not an inherent feature of lymphocytes from the SHR model of genetic hypertension. We propose that the activity of the

This study was designed to determine the cytoplasmic pH (pH,) profile of lymphocytes from a rat model of genetic hypertension that is well suited for study before and after the development of spontaneous hypertension. For this purpose, pHj was measured in thymic lymphocytes obtained from spontaneously hypertensive rats (SHR) and from age-matched Wistar-Kyoto (WKY) control rats using 2',7'-bis carboxyethyl-5,6-carboxyfluorescein (BCECF), a pHsensitive fluorescence probe. At the age of 16-20 weeks, pH, of lymphocytes suspended in a HCOj-free HEPES-buffered solution, was markedly lower in the SHR than in the WKY rats (7.07±0.02,7i=16 and 7.22±0.01, n=15, respectively,p<0.001), whereas systolic blood pressure was higher in SHR than in WKY rats (175±5.0 and 105±3.0 mm Hg, respectively,p<0.001). In rats less than 5 weeks of age, pH, was also lower in SHR than in WKY rat lymphocytes (7.12±0.04, n = l l and 7.23±0.04, n = l l , respectively, p<0.05), although at this age systolic blood pressure was not different between the two groups (87±4.0 and 85±3.0 mm Hg, respectively). In lymphocytes suspended in a more physiological HCO 3 /CO 2 -buffered solution, pHj was again lower in the adult SHR than in the WKY rat (7.18±0.02, n=U and 7.31 ±0.02, n=16, respectively,p<0.001). Under this condition, blockade of Na + -H + exchange by a specific inhibitor, ethyl-isopropyl-amiloride (EIPA), or by exposure to Na + -free media resulted in intracellular acidification in both SHR and WKY rat lymphocytes. The difference in pH ; between SHR and WKY rat lymphocytes persisted after blockade of the Na + -H + exchanger by either EIPA (7.09 ±0.04 vs. 7.20+0.03, p< 0.05) or by removal of external Na + (7.04 ±0.05 vs. 7.19±0.02,/;<0.005). Our data show that reduced pH, is a feature of lymphocytes from the SHR that is apparent before and after the development of hypertension. Persistence of reduced pHj in SHR cells, as compared with WKY rat cells, after Na + -H + blockade suggests that a primary abnormality in the activity of the Na + -H + exchanger is unlikely to account for the observed reduction in steady-state pH : of SHR cells. This alteration in pHj regulation persisted after removal of external Na + and was seen in the presence and in the absence of external HCO 3 , indicating that a sodium-independent, bicarbonate-independent mechanism of cytoplasmic acid accumulation accounts for the observed difference in pH,. (Hypertension 1990;15:97-103)

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