Renal interstitial fluid Ca(2+) concentration ([Ca(2+)](isf)) was measured in anesthetized Wistar rats by using in situ microdialysis. During perfusion of 20 cm of the proximal small intestine with Ca(2+)-free buffer, renal [Ca(2+)](isf) was 1.63 +/- 0.19 mmol/l in the cortex (n = 6) and 1.93 +/- 0.12 mmol/l in the medulla (n = 5, P = 0.223). When Ca(2+) in the intestinal lumen was increased to 3 mmol/l, no change was seen in total or ionized serum Ca(2+) (S(Ca)), urinary Ca(2+) excretion (U(Ca)), or Ca(2+) in a microdialysate of the kidney cortex. Increasing intestinal Ca(2+) further, to 6 mmol/l, was without effect on S(Ca) but significantly increased U(Ca) by 38% and microdialysate Ca(2+) by 36% (1.25 +/- 0.0.09 vs. 1.70 +/- 0. 14 mmol/l, n = 4, P < 0.05). Intravenous infusion of 28 ng. kg(-1). min(-1) of parathyroid hormone for 1 h during perfusion of the intestinal lumen with 1 mmol/ Ca(2+)caused a 7-10% rise in S(Ca), a 40% fall in U(Ca), and a 32% increase in microdialysate Ca(2+) (1.32 +/- 0.13 vs. 1.74 +/- 0.13 mmol/l, n = 6, P < 0.05). Interlobar arteries with a mean diameter of 120 microm were studied by using a wire myograph to determine whether changes in extracellular Ca(2+) affect muscle tone. When precontracted with 5 micromol/l serotonin, the arteries relaxed in response to cumulative addition of Ca(2+) (1-5 mmol/l) with an ED(50) value for Ca(2+) of 3.30 +/- 0.08 mmol/l, n = 3. These data demonstrate that [Ca(2+)](isf) changes dynamically during manipulation of whole-animal Ca(2+) homeostasis and that intrarenal arteries relax in response to extracellular Ca(2+) varied over the range measured in vivo.

We recently described a perivascular sensory nerve-linked dilator system that can be activated by interstitial Ca2+([Formula: see text]). The present study tested the hypothesis that [Formula: see text] in the rat duodenal submucosa varies through a range that is sufficient to activate this pathway. An in situ microdialysis method was used to estimate [Formula: see text]. When the duodenal lumen was perfused with Ca2+-free buffer, [Formula: see text] was 1.0 ± 0.13 mmol/l. [Formula: see text] increased to 1.52 ± 0.04, 1.78 ± 0.10, and 1.89 ± 0.1 when the lumen was perfused with buffer containing 3, 6, and 10 mmol/l Ca2+, respectively ( P < 0.05).[Formula: see text] was 1.1 ± 0.06 mmol/l in fasted animals and increased to 1.4 ± 0.06 mmol/l in free-feeding rats ( P < 0.05). Wire myography was used to study isometric tension responses of isolated mesenteric resistance arteries. Cumulative addition of extracellular Ca2+-relaxed serotonin- and methoxamine-precontracted arteries with half-maximal effective doses of 1.54 ± 0.05 and 1.67 ± 0.08 mmol/l, respectively ( n = 5). These data show that duodenal[Formula: see text] undergoes dynamic changes over a range that activates the sensory nerve-linked dilator system and indicate that this system can link changes in local Ca2+ transport with alterations in regional resistance and organ blood flow.

The mfuslon of L-argmme mduces the productron of mtrtc oxrde and sttmulates the immediate secretron of msuhn To examme the relatronshrp between msulm reststance and endothelmm-dependent vascular relaxatton m patrents with essential hypertension, we evaluated the renal and msulm responses to L-argmme, 500 mg/kg infused mtravenously over 30 mmutes, m 23 patients with mild essenttal hypertensron who were neither obese nor diabetic and m 20 normotenstve control subJects We found no difference between the two groups m blood glucose or msulm m the fasting condrtton The renovascular relaxatron mduced by L-argmme was srgmficantly less m patients with essential hypertension than m normotensrve control subJects The mcrease m plasma cychc GMP in response to L-arginine was lower m hypertensive patients than m normotensive SubJeCtS Although the serum concentrattons of glucose m response to L-argmme were smular m the two groups, the serum msulm response of me essenhal hypertensrves was srgmficantly hrgher than that of the normotensive subJects In all subJects, the peak cychc GMP response to L-argmme was srgmficantly correlated wtth the peak Aglucose/ Amsulm ratto response to L-argmme (r= 69, P< 001) Fmdmgs suggested that an impanment of endothehum-dependent renal vascular relaxation and a reduced sensrtrvtty to msulm are present m patients with essential hypertension A lmk may be present between the abnormahty of the L-argmmelmtrrc oxide/cyclic GMP pathway and msulm resistance m patients with essential hypertension (Hypertension. The vasodilatory effect of msulm is reportedly mediated by the stimulation of the release of NO.26127 If so, there should be a dtrect physiologrcal correlation between msulm resistance and vascular endothehal dysfunction m patients with essential hypertension The mfusion of L-argmme induces the production of NO-cGMP and sttmulates the immediate secretron of msulm. An elevated plasma level of argmme is a particularly potent stimulus for insulin secretion, although the mechanism 1s not completely known 2829 We examined the responses to renal ctrculation and glucose/msulm to infused L-argmme to evaluate the relattonshtp between rnsulrn sensrtrvtty and endothebal function in patients with essential hypertension Subjects MethodsWe studied 23 Japanese mpattents with mild to moderate essential hypertension (16 males and 7 females, mean age 47 -t-3 years) and 20 normotensive control subJects (14 males and 6 females, mean age 4522 years) Hypertension was defined as a systolic or diastolic blood pressure of more than 160 mm Hg or/and 95 mm Hg, determmed m stttmg posmon on at least three different occastons Measurements were obtained m the outpatient clmtc of Hiroshima University School of Medrcme Patients with secondary forms of hypertenston were excluded by the appropriate chmcal and btochemtcal exammatrons None of the pattents had a hrstory of cardiovascular or cerebrovascular disease, drabetes melhtus, hypercholesterolemla, hver dtsease, or renal dtsease Normotenston was defined as a systohc blood ...

by a high plasma concentration of vasopressin, exogenous vasopressin-induced hyperpressor action and cardiac hypertrophy. We proposed that hypertension in BHR is caused by an abnormality in vasopressin-mediated vasoconstriction.There are several lines of evidence showing that vasopressin plays an important role in the development and maintenance of hypertension in spontaneously hypertensive rats (SHR) (2-7). Naitoh et al. (8) reported the involvement of vasopressin V1 receptor-mediated pressor action in the pathogenesis of hypertension in SHR. On the other hand,

The regulation of the intracellular concentration of Mg2+ ([Mg2+]i) is not fully understood. The level of Mg in lymphocytes is a good predictor of total body Mg status. We measured [Mg2+]i and total Mg in rat lymphocytes by using, respectively, the fluorescent Mg2+ indicator mag-fura-2 and atomic absorption spectrophotometry. The basal [Mg2+]i in rat lymphocytes was 328 +/- 23 micromol/l. An elevation to 5 mmol/l or the removal of extracellular Mg2+ did not affect [Mg2+]i. A reduction in extracellular Na+ did not influence [Mg2+]i for 60 min. The total Mg concentration in lymphocytes also remained stable. Results suggest that the permeability of the plasma membrane to Mg2+ is very low, and that Na+/Mg2+ exchange is not involved in the regulation of [Mg2+]i in rat lymphocytes.