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Biomedical subjects

L Poston

Publications and source records attributed to L Poston.

At least 109 records · Page 6Linked to original sources
PubMed1994

Prevention by insulin treatment of endothelial dysfunction but not enhanced noradrenaline-induced contractility in mesenteric resistance arteries from streptozotocin-induced diabetic rats.

1. Streptozotocin-induced diabetic rats (Wistar) were implanted with sustained release insulin pellets (release rate = 4 u day-1) or with placebo pellets (palmitic acid) from the onset of glycosuria. 2. Noradrenaline sensitivity, endothelium-dependent relaxation to acetylcholine and endothelium-independent relaxation to sodium nitroprusside were assessed in mesenteric resistance arteries from the insulin-treated (IT) diabetic animals and compared to placebo-implanted (PI) diabetics and age-matched controls. 3. Arteries from PI-diabetic rats (8-10 weeks) demonstrated an enhanced maximal response to noradrenaline compared to controls, which was not prevented by insulin treatment (control 2.65 +/- 0.17 mN mm-1, n = 18 arteries versus PI-diabetic 3.73 +/- 0.40 mM mm-1, n = 5, P < 0.05; control versus IT-diabetic 4.02 +/- 0.19 mN mm-1, n = 22, P < 0.001). Sensitivity to noradrenaline was similar between the three groups. 4. In the presence of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), IT and PI arteries were more sensitive to noradrenaline than control arteries (pEC50: control 5.75 +/- 0.08, n = 17, versus PI-diabetic 6.14 +/- 0.09, n = 8, P < 0.05; control versus IT-diabetic 6.38 +/- 0.08, n = 20, P < 0.001). 5. The maximum contractile response to depolarizing 125 mM K+ was significantly enhanced in IT-diabetic arteries but not PI-diabetic when compared to control arteries (maximum response: control 3.74 +/- 0.15 mN mm-1, n = 18, versus PI-diabetic 3.61 +/- 0.19 mN mm-1, n = 11, NS; control versus IT-diabetic 4.66 +/- 0.18 mN mm-1, n = 22, P < 0.001). 6. Endothelium-dependent relaxation to acetylcholine was profoundly impaired in the PI-diabetic arteries, but in the IT-diabetic arteries was not significantly different from controls (pEC50: control 7.64 +/- 0.19, n = 17, versus PI-diabetic 6.07 +/- 0.12, n = 8, P < 0.001; control versus IT-diabetic 7.36 +/- 0.09, n = 22, NS). 7. Endothelium-independent relaxation to sodium nitroprusside was slightly but significantly impaired in the PI-diabetic arteries, but was not significantly different in the IT-diabetic arteries compared to controls (pEC50: control 7.78 +/- 0.10, n = 13, versus PI-diabetic 7.31 +/- 0.13, n = 13, P <0.05; control,versus IT-diabetic 7.64 +/- 0.09, n = 16, NS).

Acetylcholine↗
PubMed1994

Endothelial function in the isolated perfused mesentery and aortae of rats with streptozotocin-induced diabetes: effect of treatment with the aldose reductase inhibitor, ponalrestat.

1. Noradrenaline sensitivity and relaxation to acetylcholine were investigated in the isolated perfused mesentery and in aortic rings of control and streptozotocin (STZ)-induced (50 mg kg-1) diabetic Charles River rats. 2. In addition, noradrenaline sensitivity and acetylcholine relaxation were similarly assessed in streptozotocin-induced diabetic rats treated from the time of onset of diabetes with the aldose reductase inhibitor, ponalrestat (100 mg kg-1 day-1). 3. The untreated diabetic rats (2-10 weeks after injection of STZ) demonstrated enhanced vascular sensitivity to noradrenaline in the perfused mesenteric arterial tree, compared with age matched controls (pEC50 [-log concentration (M)]: diabetic 5.62 +/- 0.09, n = 18, versus control 5.23 +/- 0.07, n = 16, P < 0.01). 4. Acetylcholine-induced relaxation was significantly impaired in the perfused mesentery of the diabetic animals compared to controls (pED50 [-log dose (mol)]: diabetic 9.87 +/- 0.10, n = 20, versus controls, 10.29 +/- 0.09, n = 20, P < 0.05). 5. In contrast, the aortic ring preparations demonstrated no significant functional differences between the diabetic and control groups in response to either noradrenaline (pEC50: diabetic 7.66 +/- 0.08, n = 15, versus controls 7.55 +/- 0.06, n = 15, NS), or acetylcholine (pEC50: diabetics 7.30 +/- 0.06, n = 15, versus controls 7.40 +/- 0.09, n = 15, NS). 6. Treatment with the aldose reductase inhibitor, ponalrestat, did not affect the increased vascular reactivity to noradrenaline, or impaired relaxation to acetylcholine in the perfused mesentery.

Acetylcholine↗
PubMed1994

The effect of hyperglycaemia on function of rat isolated mesenteric resistance artery.

1. Noradrenaline sensitivity and acetylcholine-induced relaxation were investigated in mesenteric resistance arteries from female Wistar rats (220-250 g) following exposure to isotonic supraphysiological glucose solutions (20 and 45 mM, in physiological buffer, 2 h incubation). 2. Arteries incubated in 20 mM glucose demonstrated enhanced noradrenaline sensitivity compared with those in physiological buffer. 3. Profoundly impaired endothelium-dependent relaxation to acetylcholine was observed in arteries incubated in 20 and 45 mM glucose. 4. Indomethacin (10 microM) normalized noradrenaline sensitivity in 20 mM glucose, but unmasked an enhanced maximum response in 20 and 45 mM glucose relative to controls. 5. Addition of L-arginine (0.1 mM) prevented the abnormality of acetylcholine-induced relaxation in the 20 mM glucose medium and significantly improved relaxation in 45 mM glucose. 6. The aldose reductase inhibitor, ponalrestat (10(-5) M, ZENECA Pharmaceuticals), prevented impaired acetylcholine-mediated relaxation in 20 mM glucose and significantly improved relaxation in 45 mM glucose. 7. Indomethacin (10 microM) improved maximum relaxation but did not alter impaired sensitivity to acetylcholine in the high glucose media (20 and 45 mM). 8. Superoxide dismutase (SOD, 150 u ml-1) also prevented impaired acetylcholine-induced relaxation in 20 mM glucose but not in 45 mM glucose. 9. Endothelium-independent relaxation to sodium nitroprusside (SNP, 10(-9)-10(-5) mM) was normal in 20 mM glucose but was slightly, although significantly impaired by 45 mM glucose. 10. Enhanced responsiveness of rat isolated mesenteric resistance arteries to noradrenaline caused by elevated glucose would appear to be mediated through abnormal cyclo-oxygenase activity and the reduced tonic release of nitric oxide. 11. Hyperglycaemia may lead to abnormal endothelium-dependent relaxation in these arteries through several mechanisms which include a role for increased free radical production, polyol pathway activation and altered L-arginine metabolism.

Animals↗
PubMed1994

Dietary sodium intake, airway responsiveness, and cellular sodium transport.

Both epidemiologic and experimental evidence suggest that a high dietary sodium intake may increase airway responsiveness, but no adequate explanation exists of how changes in sodium intake might lead to increased responsiveness. This investigation was carried out to study dietary sodium intake and airway response to methacholine in relation to cellular sodium transport in 52 young men. Airway response to methacholine was associated with urinary sodium excretion when subjects were on normal sodium intake. Airway responsiveness in patients with mild asthma correlated with the furosemide-insensitive influx of sodium into peripheral leukocytes stimulated by autologous serum, but there was no relation between this influx and 24-h urinary sodium excretion. In a separate investigation, serum from subjects with increased airway responsiveness caused an increase in the sodium influx and sodium content of leukocytes from nonatopic subjects. The magnitude of the furosemide-insensitive, serum stimulated influx was related to the degree of airway responsiveness of the serum donor, as was the increase in intracellular sodium content. Neither was related to the 24-h urinary sodium excretion of the donor. Patients with airway hyperresponsiveness have an increased sodium influx into cells stimulated by a serum-borne factor. This is independent of the effect of added dietary sodium on airway responsiveness.

Adolescent↗
PubMed1994

Resistance artery morphology in essential hypertension and in normal subjects: some methodological considerations.

Although it is generally assumed that small arteries are truly isometric when studied in a myograph, these arteries significantly shorten during the normalisation procedure. We assessed the effects of this shortening on calculation of morphological variables in small arteries using vessel length before and after normalisation. Subcutaneous resistance arteries were dissected from gluteal biopsies obtained from normotensive subjects (n = 7, supine pressure 116/69 +/- 5/3(SE) mmHg, internal artery diameter 276 +/- 16 microM) and patients with essential hypertension on no treatment (n = 13, supine pressure 160/102 +/- 4/2 mmHg, internal diameter 256 +/- 9 microM) mounted on a small vessel myograph. Using the actual shortened 'normalised' length compared with measurement using the original artery length, media thickness was significantly greater both in normal subjects (24.0 +/- 2.7 microM vs. 22.7 +/- 2.7 microM, 2 P < 0.05, paired t-test) and in hypertensives (27.6 +/- 1.5 microM vs. 26.5 +/- 1.4 microM, 2 P < 0.001). Calculated from the actual shortened 'normalised' length vs. original artery length, media:lumen ratio was also increased in the normal subjects (8.6 +/- 0.6 vs. 8.2 +/- 0.6 2 P < 0.05) and in the hypertensives (11.2 +/- 0.7 vs. 10.7 +/- 0.7, 2 P < 0.001). For the media thickness in normal subjects this was an increase of 6% (95% CI: 1-12%) and in hypertensives of 4% (95% CI: 2-6%). Standard methods for study of small arteries underestimate media thickness and media:lumen ratio in normal subjects and in hypertensives.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Carbon dioxide induced vasorelaxation in rat mesenteric small arteries precontracted with noradrenaline is endothelium dependent and mediated by nitric oxide.

Hypercapnia induces initial constriction and prolonged relaxation of rat small mesenteric arteries. The mechanism of the relaxation is unknown, but has been attributed to lowering of pHi in the vascular smooth muscle. In this study we have investigated the response to raised PCO2 at constant pHo, in mesenteric small arteries precontracted with noradrenaline. 10% CO2 led to a fall in pHi associated with acute potentiation of tension, and subsequent relaxation. The relaxation did not occur in arteries in which the endothelium had been removed, nor in arteries pretreated with the nitric oxide synthase inhibitor, L-NAME (10(-4)M, NG-nitro-L-arginine methyl ester). The D-enantiomer, D-NAME, was without effect. We conclude that hypercapnic-induced vasodilatation in this circulation occurs via endothelium derived nitric oxide production.

Amino Acid Oxidoreductases↗
PubMed1993

Abnormal endothelial cell function of resistance arteries from women with preeclampsia.

OBJECTIVE: There is substantial indirect evidence that the vascular endothelium may be dysfunctional in preeclampsia and that reduced production of endothelial-derived vasodilators may account for the increased vascular resistance and enhanced pressor sensitivity characteristic of this disorder. In this study we directly investigated endothelial function by examining acetylcholine-mediated relaxation in small arteries dissected from the subcutaneous fat layer examined at the time of cesarean section. STUDY DESIGN: By means of a small vessel myograph we measured tension in resistance arteries of normal pregnant women (n = 12) and women with preeclampsia (n = 12) and assessed the contributions of vasodilatory prostanoids and endothelium-derived relaxing factor to endothelium-dependent relaxation, as elicited by acetylcholine, 1 nmol/L to 10 mumol/L, after precontraction with 3 mumol/L norepinephrine. RESULTS: Endothelium-dependent relaxation was impaired in arteries of women with preeclampsia compared with arteries from normotensive pregnant women. Endothelium-independent relaxation as assessed by sodium nitroprusside was not altered in the arteries from preeclamptic women. CONCLUSIONS: This study provides direct evidence of abnormal endothelial function in preeclampsia. No deficiency in endothelium-independent relaxation could be detected.

Acetylcholine↗
PubMed1993

Effects of sodium-transport inhibition in human resistance arteries.

It is hypothesized that endogenous inhibitors of active sodium transport may lead to an increase in peripheral vascular resistance. From studies in animal conduit arteries there is substantial evidence that cardiac glycosides may increase tension. A number of studies from our laboratory demonstrate that inhibition of active sodium transport may also increase tension in human resistance arteries, and that reduced Ca efflux via Na/Ca exchange could be a contributory mechanism. Further experiments also have suggested that endogenous inhibitors of sodium transport could lead to an increase in peripheral vascular resistance by reducing endothelium-dependent relaxation.

Arginine↗
PubMed1993

Beta-adrenoceptor agonist mediated relaxation of rat isolated resistance arteries: a role for the endothelium and nitric oxide.

1. Isoprenaline (10(-9)-10(-5) M) relaxed rat isolated mesenteric resistance arteries pre-contracted with K+ (30-60 mM) (p EC50 (M) 8.03 +/- 0.40; maximum relaxation 66.79 +/- 2.43%, n = 7). This relaxation was partially attenuated by the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 10(-4) M). 2. The beta 2-adrenoceptor agonist, salbutamol (10(-9)-10(-5) M), produced a modest maximum relaxation (35.93 +/- 2.93%), which was not sensitive to L-NAME. 3. The beta 1-adrenoceptor agonist, dobutamine (10(-9)-10(-5) M), relaxed arteries precontracted with K+. This relaxation was abolished by L-NAME (10(-4) M) and also by propranolol (10(-6) M), but not affected by D-NAME (10(-4) M). The inhibition by L-NAME was partially reversed by L-arginine (10(-3) M). Removal of the endothelium severely attenuated relaxation to dobutamine. 4. Contractile responses to depolarizing K+ solutions were enhanced by the addition of L-NAME, and also by removal of the endothelium. 5. The above findings demonstrate that beta 1-adrenoceptor causes relaxation via NO release from the endothelium of rat mesenteric resistance arteries. In addition, contraction to K+ is modified by release of NO from the endothelium, possibly in response to tension development.

Adrenergic beta-Agonists↗
PubMed1993

Human lymphocyte sodium-hydrogen exchange. The influences of lipids, membrane fluidity, and insulin.

The relation between serum lipids, membrane fluidity, insulin, and the activity of the sodium-hydrogen exchanger was investigated in human lymphocytes from 83 subjects. Subjects had a wide range of serum lipids and no concurrent disease. Lymphocyte membrane anisotropy (inversely related to membrane fluidity) was measured with a fluorescence polarization method. Sodium-hydrogen exchange maximal proton efflux rate, affinity for external sodium, and resting pH were determined with the intracellular pH-sensitive fluorochrome 2',5'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Sodium-hydrogen exchange maximal proton efflux rate was negatively correlated with the age of the subject (p = 0.03). Membrane anisotropy correlated with serum triglyceride (p = 0.04). Multiple regression analysis demonstrated that the maximal proton efflux rate in human lymphocytes was significantly related to age (p = 0.005), systolic blood pressure (p = 0.04), membrane anisotropy (p = 0.03), and serum cholesterol (p = 0.03). Incubation of lymphocytes with insulin failed to affect sodium-hydrogen exchange kinetics, intracellular buffering power, or resting intracellular pH. These results suggest that membrane-bound transport proteins may be influenced by serum lipids and the fluidity of the lipid membrane in which they are bound, but they are unlikely to be affected by insulin.

Adult↗
PubMed1992

Effect of bufalin and pregnanes on vasoreactivity of human resistance arteries.

Endogenous Na/K ATPase inhibitory activity has been implicated in salt and water homeostasis in mammals and amphibians. Recent interest has focused on endogenous cardiac glycosides, some progesterone derivatives (pregnanes) and the amphibian bufodienolides. This study has examined the effects of non-planar and planar pregnanes and the bufodienolide bufalin on vasoreactivity of human resistance arteries. Bufalin and a non-planar pregnane caused concentration-dependent potentiation of the tone of submaximally pre-contracted arteries and inhibited endothelium-dependent relaxation, whereas a planar pregnane affected neither response. The relative potency of the compounds studied suggest the results do not simply reflect degrees of Na/K ATPase inhibition. The active compounds may be important in the regulation of vascular tone.

Acetylcholine↗
PubMed1992

Basal metabolic rate in adults with growth hormone deficiency and in patients with acromegaly: relationship with lean body mass, plasma insulin level and leucocyte sodium pump activity.

1. The relationship of lean body mass, plasma insulin concentration and leucocyte active sodium transport with basal metabolic rate was investigated in 24 adults with growth hormone deficiency before and after treatment with recombinant human growth hormone and in 10 patients with untreated acromegaly. 2. Based on total-body potassium determined by whole-body 40K counting, patients with acromegaly had increased lean body mass, whereas lack of growth hormone was associated with decreased lean body mass. 3. By indirect calorimetry, patients with acromegaly had increased basal metabolic rates and patients with growth hormone deficiency had decreased values when expressed as percentages of values predicted from the WHO/FAO/UNU equations. Basal metabolic rate expressed in terms of lean body mass was similar in acromegaly and growth hormone deficiency, but was higher than normal in both patient groups. 4. The leucocyte ouabain-sensitive sodium efflux rate constant was decreased in both patients with acromegaly and patients with growth hormone deficiency, and there was no correlation with basal energy expenditure, fasting plasma insulin level or serum growth hormone level. 5. There was no increase in the sodium efflux rate constant in patients with growth hormone deficiency after 1 month on treatment with recombinant human growth hormone. 6. Apparent differences in basal metabolic rate in growth hormone deficiency and acromegaly are due to changes in lean body mass. Both adults with growth hormone deficiency and patients with acromegaly have increased energy expenditure, probably owing to changes in fuel metabolism which are not reflected in the leucocyte sodium pump activity.

Acromegaly↗
PubMed1992

Endothelium-dependent relaxation and noradrenaline sensitivity in mesenteric resistance arteries of streptozotocin-induced diabetic rats.

1. Noradrenaline sensitivity and acetylcholine-induced relaxation were investigated in mesenteric resistance arteries of control and streptozotocin-induced diabetic rats. 2. The diabetic rats demonstrated enhanced vascular sensitivity to noradrenaline compared with age-matched controls (pEC50 5.99 +/- 0.06 for diabetic rats, n = 25, versus 5.82 +/- 0.03 for controls, n = 45, P < 0.05). 3. Significant impairment of acetylcholine-induced relaxation was observed in arteries from the diabetic animals compared with controls (pEC50 6.81 +/- 0.17 for diabetic rats, n = 21, versus 7.54 +/- 0.17 for controls, n = 45, P < 0.001). 4. The difference between acetylcholine-induced relaxation in diabetic and control arteries remained in the presence of 10 microM indomethacin (pEC50 6.41 +/- 0.11 for diabetic rats, n = 16, versus 7.59 +/- 0.08 for controls, n = 20, P < 0.001). 5. The nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA, 1 mM) produced profound inhibition of acetylcholine-induced relaxation in diabetic arteries but partial inhibition in controls. The incomplete inhibition of acetylcholine-induced relaxation by L-NMMA in the control arteries was the result of ineffective inhibition of nitric oxide synthase since an alternative inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 0.1 mM), led to similar inhibition to that seen in the diabetic arteries with L-NMMA. The endothelium-derived relaxing factor (EDRF)-mediated component of acetylcholine-induced relaxation determined by use of the nitric oxide synthase inhibitors was, therefore, apparently reduced in diabetic rats compared with control animals.6. In further experiments L-NAME was found to enhance the response to noradrenaline in control rats but not in diabetic animals, suggesting that the abnormal response to noradrenaline in the diabetic animals was also due to reduced EDRF release.7. Nitroprusside-induced relaxation (endothelium-independent) was similar in arteries from control anddiabetic rats (pEC5o 7.61 +/- 0.13 for diabetic arteries, n = 18, versus 7.68 +/- 0.15 in the controls, n = 20, P not significant).8. These results suggest that endothelial function is abnormal in mesenteric resistance arteries of streptozotocin-induced diabetic rats and that this is predominantly due to reduced EDRF release.

Acetylcholine↗
PubMed1991

Low-concentration ouabain does not inhibit noradrenaline-induced contraction of human resistance arteries.

1. Using a Mulvany-Halpern myograph to measure changes in isometric tension, we have investigated the effect of ouabain on noradrenaline-induced contraction of human subcutaneous resistance arteries. 2. Low concentrations of ouabain (10 nmol/l or less) were shown not to alter vascular smooth muscle contractility or sensitivity to noradrenaline. 3. In contrast, higher concentrations of ouabain (100 nmol/l or more) were found to depress vascular smooth muscle contractility and to reduce the sensitivity of the noradrenaline concentration-response relationship. 4. These findings may have implications regarding the presence of an endogenous inhibitor of the sodium pump in essential hypertension and in pregnancy-associated hypertension.

Arteries↗
PubMed1991

The in vitro effects of griffonin and ouabain on erythrocyte sodium content obtained from normal subjects and sickle cell patients.

The in vitro effects of griffonin and ouabain on erythrocyte sodium content have been investigated in 6 normal subjects and 6 sickle cell patients. Intracellular sodium contents of normal or sickle cells incubated for 8 h in tris buffer, griffonin/tris buffer, or ouabain/tris buffer were determined. Incubation of normal cells in tris buffer or 0.5 mmol/l griffonin had little effect on the cell sodium content. However, 1.0 mmol/l griffonin/tris buffer raised the cell sodium level (P less than 0.05) over the incubation period. Ouabain/tris buffer (0.5 mmol/l or 1.0 mmol/l) also raised the sodium content (P less than 0.05 to P less than 0.001). Incubation of sickle cells in tris buffer raised the cell sodium (P less than 0.05) as did 0.5 mmol/l or 1.0 mmol/l griffonin (P less than 0.05 to P less than 0.001). Ouabain/tris buffer (0.5 mmol/l or 1.0 mmol/l) raised the intra-erythrocyte sodium level (P less than 0.01 to P less than 0.001). These findings suggest that ouabain and griffonin both have similar actions on intra-erythrocyte sodium content although ouabain was more potent. It is suggested therefore that griffonin could be a useful anti-sickling drug for sickle cell disease crisis.

Acetonitriles↗
PubMed1991

Leucocyte intracellular pH and Na(+)-H+ exchange activity in essential hypertension: an in vitro study under physiological conditions.

The cellular basis for essential hypertension remains obscure. Abnormal ion transport has been demonstrated in both experimental and essential hypertension, raised levels of sodium-lithium (Na(+)-Li+) and sodium-proton (Na(+)-H+) exchange in blood cells being a consistent feature. However, Na(+)-H+ exchange is not the main regulator of intracellular pH at resting pH, while the importance of the contribution of bicarbonate to cellular pH regulation is now increasingly appreciated. Serum and serum-derived growth factors are known to affect intracellular pH and the activity of the Na(+)-H+ antiporter. This study was designed to investigate the activity of Na(+)-H+ exchange in the leucocytes of patients with essential hypertension in the presence of bicarbonate in vitro and to measure the effect of autologous serum on intracellular pH and Na(+)-H+ exchange. Paired serum samples from essential hypertensives and their controls were used on leucocytes from other (unrelated, normotensive) donors to investigate the same parameters. In a study of 30 patients with untreated essential hypertension and 30 controls matched for age, sex, race and body habitus we found no difference in resting pH or buffering capacity (pH 7.28 +/- 0.01 and 32.0 +/- 1.6 mmol/l per pH, hypertensives, versus 7.27 +/- 0.02 and 34.5 +/- 1.8 mmol/l per pH, controls) but a marked difference in the maximal rate of Na(+)-H+ exchange in response to intracellular acidification (57.8 +/- 3.2 mmol/l per min versus 47.2 +/- 1.4 mmol/l per min, P = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effect of ouabain on endothelium-dependent relaxation of human resistance arteries.

Inhibition of active sodium transport by ouabain was found to cause concentration- and time-dependent impairment of acetylcholine-induced relaxation in human resistance arteries with a significant effect at 100 pM. The reduced acetylcholine response was attributable to inhibition of the NG-monomethyl L-arginine-sensitive but not the indomethacin-sensitive component of relaxation. Relaxation by sodium nitroprusside was not affected by ouabain, suggesting that inhibition of sodium transport, directly or indirectly, must affect synthesis or release of endothelium-derived relaxing factor rather than its effector pathway. These results do not support the existence of an additional endothelium-derived relaxing factor other than endothelium-derived relaxing factor, which is dependent on sodium pump activity. The finding that inhibition of sodium transport has a profound effect on vascular relaxation may have implications in the pathogenesis of certain forms of hypertension.

Acetylcholine↗