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Biomedical subjects

M Feuring

Publications and source records attributed to M Feuring.

At least 19 recordsLinked to original sources
PubMed2005

Aldosterone blunts human baroreflex sensitivity by a nongenomic mechanism.

BACKGROUND: Impaired baroreflex sensitivity (BRS) is a negative predictive factor of mortality in cardiovascular disease. Aldosterone has been shown to decrease BRS in humans and animal models. However, the mode of aldosterone action, whether genomic or nongenomic has not been determined. Therefore, we conducted a clinical study to examine whether BRS, as measured by the phenylephrine method, is impaired in humans by aldosterone by a nongenomic mechanism. METHODS: In a randomised, double-blinded, fourfold cross-over trial in 16 healthy male volunteers, BRS was tested 15 minutes after initiation of a continuous infusion of aldosterone (3 microg/minute) or placebo. 6 hours earlier, this period was preceded by an injection of either canrenoate (400 mg) or placebo. RESULTS: BRS was 34.6 +/- 4.7 ms/mm Hg in the placebo/placebo period. It was significantly blunted in the placebo/aldosterone (25.5 +/- 1.8 ms/mm Hg) as well as in the canrenoate/placebo (24.0 +/- 1.5 ms/mm Hg) and the canrenoate/aldosterone (25.4 +/- 2.5 ms/mm Hg) periods. CONCLUSION: These data suggest that the decreased BRS caused by aldosterone is due to a rapid, thus presumably nongenomic mechanism, as these effects occur in a time frame that excludes genomic aldosterone effects at large. The mineralocorticoid receptor (MR) antagonist canrenoate does not block these effects, but blunts BRS by itself.

Adult↗
PubMed2005

Impact of ABO blood groups on tirofiban mediated inhibition of platelet function.

Previous investigations revealed that ABO blood groups are associated with divergent concentrations of several coagulation factors. Concentrations of von Willebrand factor (vWF) and factor VIII are lower in individuals with blood group O as compared to subjects with blood group A, B or AB which might result in a reduced inhibition of platelet aggregation. The aim of the present in-vitro-investigation was to elucidate the impact of ABO blood group dependent vWF concentrations on tirofiban mediated inhibition of GPIIb/IIIa function. Platelet function was measured with the platelet function analyzer PFA-100 at baseline and at increasing concentrations of tirofiban and stratified for blood group O vs. A. If measured with the collagen/epinephrine cartridge, blood group O was associated with a prolonged mean baseline closure time in comparison with blood group A (175.8 +/- 64.9 s vs. 121.4 +/- 33.4 s, p = 0.037) which was paralleled by reduced concentrations of vWF and factor VIII. In contrast, no differences in closure time (227.6 +/- 76.1 s vs. 223.9 +/- 81.9 s, p = 0.96) could be found in the presence of tirofiban (0.1 microg/ml). Thus, tirofiban mediated GP IIb/IIIa receptor antagonism as determined with the PFA-100 seems to be independent on plasma concentration of vWF.

ABO Blood-Group System↗
PubMed2004

Delayed genomic and acute nongenomic action of glucocorticosteroids in seasonal allergic rhinitis.

BACKGROUND: Glucocorticosteroids are effective in the treatment of allergic rhinitis, a disease characterized by a variety of symptoms, e.g. rhinorrhea and itching. The time course of symptomatic relief for allergic rhinitis by steroids has not been examined in detail to date, although the onset of steroid action is one of the main discriminations between genomic and nongenomic actions of steroids. We therefore investigated the time course of subjective and objective measures of nasal affection after steroid administration in patients with allergic rhinitis following specific allergen challenge. METHODS: Six female and 18 male volunteers (median age 26 years) with a history of allergic rhinitis but currently free of symptoms were included in this randomized, placebo-controlled, double-blind, three-period crossover study. A single dose of either betamethasone (60 mg), methylprednisolone (400 mg) or placebo was given intravenously, 5 min after intranasal allergen provocation. After 10, 20, 60, 150 and 240 min, nasal itching and nasal obstruction were assessed using a standardized visual analogue scale. In addition, nasal airflow was measured by anterior rhinomanometry. RESULTS: Nasal itching was markedly reduced following either of the two steroids within 10 min after administration of study drug. Itching was depressed by 38% following betamethasone (P<0.05) and by 18% following methylprednisolone (P=0.07) compared with placebo. Nasal airflow and nasal obstruction were not significantly altered by steroids during the first 2 h of the study. However, after 150 min, nasal airflow was 21% rsp. 19% higher after methylprednisolone and betamethasone (P<0.05) compared with placebo. After 240 min, nasal airflow was increased by 20% following betamethasone (P<0.05) and by 19% following methylprednisolone. Nasal obstruction was also beneficially affected by both steroids 150 and 240 min after administration compared with placebo (P<0.05 for both time points following betamethasone). CONCLUSION: This study for the first time shows rapid in vivo effects of external glucocorticosteroids in humans. Itching, a pathophysiologically complex sensation, is favourably influenced by steroids within 10 min, therefore presumably via nongenomic mechanisms. Though no detailed mechanisms can be derived from this study, steroid interaction with receptors in the central nervous system may play an important role in mediating this effect.

Allergens↗
PubMed2002

Bioequivalence of subcutaneous and intravenous body-weight-independent high-dose low-molecular-weight heparin Certoparin on anti-Xa, Heptest, and tissue factor pathway inhibitor activity in volunteers.

The objective of the study was to demonstrate the bioequivalence of subcutaneously (s.c.) and intravenously (i.v.) administered fixed, high-dose low-molecular-weight heparin (LMWH) on anti-activated factor X activity (anti-FXa). Secondary objectives were the analysis of the pharmacodynamic effects on Heptest, thrombin inhibition, tissue factor pathway inhibitor (TFPI), and the urinary excretion of LMWH in the randomized cross-over study following i.v. and s.c. application of 8000 anti-FXa units LMWH Certoparin in 18 healthy subjects. The bioequivalence following s.c. administration was demonstrated from the antilog of the point estimator for the application differences (s.c. minus i.v.) by an area under the activity-time curve (0-24 h) of 101% (range, 93-110%). LMWH was bioequivalent also on Heptest and TFPI, and was 50% on thrombin inhibition. The urinary excretion of biologically active material was 4.1 and 3.6% following i.v. and s.c. administration, respectively. Differences in the pharmacodynamic parameters of the assays indicate specific biological actions of high and low molecular sacharide chains of the LMWH.

Adult↗
PubMed2002

Alterations in platelet function during the ovarian cycle.

Steroid hormones may profoundly influence hemostasis; for example, as discussed for hormone replacement therapy, pregnancy and, being less obvious, for the ovarian cycle. We investigated primary hemostasis parameters using a platelet function analyzer (PFA-100) during the follicular and luteal phases in 18 healthy young women without oral contraceptives. During the follicular phase, the mean closure time (CT) was 164.7 +/- 56.7 s, and it decreased to 130.2 +/- 30.6 s in collagen/epinephrine cartridges in the luteal phase (P = 0.0095). No significant difference could be found for CT values in collagen/adenosine diphosphate cartridges during the follicular phase as compared with the luteal phase (97.2 +/- 24.2 s versus 89.6 +/- 18.4 s, P = 0.174). Negative correlations between the CT values in collagen/epinephrine cartridges and von Willebrand factor from both phases of the cycle were found (follicular phase: r = -0.53; luteal phase: r = -0.54). Fibrinogen and fibrinogen degradation products were significantly increased in the luteal phase (2.49 +/- 0.62 g/l versus 2.05 +/- 0.59 g/l and 0.12 +/- 014 versus 0.04 +/- 0.04, P = 0.02 for both parameters) as compared with the follicular phase. No significant differences could be detected for plasminogen, plasmin-antiplasmin complex, prothrombin fragment 1 + 2 and D-dimer between the groups. This study indicates that platelet function is periodically altered during the ovarian cycle due to the influence of progesterone and estrogen on von Willebrand factor concentrations.

Adult↗
PubMed2002

Seminal plasma hormone concentration after oral application of progesterone.

Previous studies have revealed beneficial in vitro effects of progesterone on sperm function. The aim of this pilot study was to prove if orally given micronized progesterone leads to elevations in progesterone and/or 17alpha-hydroxyprogesterone levels in seminal plasma, since higher seminal plasma levels of these hormones could possibly have a beneficial effect on sperm function as seen in in vitro investigations. Multiple application of micronized progesterone given over 4 days (daily dose 400 mg) to 6 healthy subjects resulted in elevated seminal plasma levels of progesterone (10.90 +/- 9.02 nmol/l vs. 1.43 +/- 0.56 nmol/l, p = 0.04) and 17alpha-hydroxyprogesterone (3.09 +/- 1.72 nmol/l vs. 1.62 +/- 1.26 nmol/l, p = 0.04) whereas no significant difference could be found in testosterone levels (34.82 +/- 13.00 vs. 30.91 +/- 8.56 nmol/l, p = 0.43). In contrast, androstendione levels in seminal plasma were reduced (2.68 1.28 nmol/l vs. 3.65 +/- 1.36 nmol/l, p = 0.01). Although micronized progesterone is rapidly metabolized, oral application resulted in pronounced elevations of progesterone and 17alpha-hydroxyprogesterone in seminal plasma. Further studies will show if oral application of micronized progesterone can induce beneficial effects on sperm function such as those seen in in vitro investigations.

17-alpha-Hydroxyprogesterone↗
PubMed2001

[Drug therapy in the old age. Drug effects in the elderly].

The frequency of multimorbidity in elderly patients may mislead the physician into practicing polypragmasy (polypharmacy), resulting in unpredictable drug interactions. Such interactions are a quite common cause of hospitalization in geriatric patients. Pharmacokinetics are often altered in the aged, and individualized medication should take into consideration not only the patient's age, liver and kidney function, but also the individual variability of hepatic metabolism and drug absorption from the gastrointestinal tract dictated by genetic polymorphism. Drug treatment in the elderly should always be carefully assessed as to its risks and benefits, and, where indicated, certain medications should be replaced by or omitted.

Age Factors↗
PubMed2001

The phosphodiesterase 4 inhibitor roflumilast is effective in the treatment of allergic rhinitis.

BACKGROUND: The beneficial effects of phosphodiesterase 4 (PDE4) inhibitors in allergic asthma have been shown in previous preclinical and clinical studies. Because allergic rhinitis and asthma share several epidemiologic and pathophysiologic factors, PDE4 inhibitors might also be effective in allergic rhinitis. OBJECTIVE: The main objective of this study was to investigate the efficacy of oral roflumilast (500 microg/day) in allergic rhinitis. METHODS: In a randomized, placebo-controlled, double-blinded, crossover study, 25 subjects (16 male, 9 female; median age, 28 years) with histories of allergic rhinitis but asymptomatic at screening received roflumilast (500 microg once daily) and placebo for 9 days each with a washout period of at least 14 days in between treatment periods. In each of the treatment periods, controlled intranasal allergen provocation with pollen extracts was performed daily beginning the third day of treatment, each time approximately 2 hours after study drug administration. Five and 30 minutes after each allergen provocation, rhinal airflow was measured by means of anterior rhinomanometry and the subjective symptoms obstruction, itching, and rhinorrhea were assessed by means of a standardized visual analog scale. RESULTS: Rhinal airflow improved almost consistently during the 9 days of roflumilast treatment, and it was significantly higher at study day 9 on roflumilast in comparison with placebo, a result also found for itching and rhinorrhea. With respect to the subjective obstruction score, a significant difference in comparison with placebo could be demonstrated within 4 days. CONCLUSION: This study shows that a PDE4 inhibitor, roflumilast, effectively controls symptoms of allergic rhinitis. Thus PDE4 inhibitors might be a future treatment option not only in allergic asthma but also in allergic rhinitis or the combination of the 2 diseases.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2001

Laboratory diagnosis of heparin-induced thrombocytopenia type II after clearance of platelet factor 4/heparin complex.

Laboratory confirmation of heparin-induced thrombocytopenia (HIT) is limited by assay sensitivity. We investigated whether laboratory confirmation can be improved after antigen clearance by determining free antibody and combining the results of antigenic and biologic assays. Blood samples were collected over 5 to 6 weeks in 14 HIT patients. As an antigenic assay, the fluorescence-linked immunofiltration assay (FLIFA) was performed, and as a biologic assay, the carbon 14-labeled serotonin release assay was performed. At day 1 when heparin was stopped, 11 of 14 patients showed positive results in both assays; thus each assay had a sensitivity of 80%. The 3 patients with negative results seroconverted in one or both assays during the subsequent 7 days. Combining the positive results of the assays increased the sensitivity to 100% at day 7, regardless of whether the antigenic or the biologic assay was performed first. Both assays became negative in all patients within 5 to 6 weeks. The sensitivity of antigen and biologic assays in HIT patients increased to 100% after the time course of the heparin-induced antibody. We assume that in some HIT patients the free antibody can be detected after withdrawal of heparin and after clearance of the platelet-factor 4/heparin complex.

Aged↗
PubMed2001

Impact of plasmapheresis on platelet hemostatic capacity in healthy voluntary blood donors detected by the platelet function analyzer PFA-100.

Previous flow cytometry studies showed that platelet activation may occur during cytapheresis, cardiopulmonary bypass and hemodialysis. The aim of this pilot study was to determine if the impact of plasmapheresis leads to alterations in platelet hemostatic capacity. Plasmapheresis was carried out in 30 volunteers using an Autopherese C (Baxter) and an MCS3p (Haemonetics). Blood samples were collected and analyzed immediately before and after plasmapheresis. As a result of the plasmapheresis on the Autopherese C, the mean closure time (CT) for collagen/epinephrine (Col/Epi) increased from 118.2 +/- 25.1 to 149.9 +/- 35.0 s and from 88.7 +/- 16.9 to 98.5 +/- 26.3 s for collagen/ADP (Col/ADP), respectively. Seven subjects showed impaired CTs after plasmapheresis for Col/Epi. For Col/ADP, five subjects showed impaired CTs after apheresis. Statistical analysis (McNemar test) showed a significant difference before and after apheresis for Col/Epi (P = 0.024) but not for Col/ADP (P = 0.088). Similar results were shown for plasmapheresis carried out with the MCS3p. These findings show that plasmapheresis can cause an impairment of platelet function in healthy volunteers as measured by the PFA-100, an effect of so far unknown clinical significance.

Adult↗
PubMed2001

Interaction of rapid nongenomic cardiovascular aldosterone effects with the adrenergic system.

Interactions between the renin-angiotensin-aldosterone system and the adrenergic system are complex and have mainly been attributed to angiotensin II, with knowledge about aldosterone action much less advanced. Only recently has evidence been forthcoming that aldosterone blunts the baroreceptor reflex and lowers heart rate variability in humans. Both effects point to an adrenergic-like action of aldosterone. It has been proposed that this blunting of baroreceptor sensitivity is mediated nongenomically and that nongenomic aldosterone action itself is modulated by the adrenergic system. The aim of the present study was to prove the hypothesis of an interaction between the autonomic nervous system and rapid, nongenomic aldosterone effects. We conducted a randomized, double blind, 8-fold cross-over trial on 18 healthy male volunteers. After pretreatment with the beta-blocking agent esmolol, the beta-agonist dobutamine, the alpha(1)-agonist phenylephrine, or placebo, placebo (0.9% NaCl) or aldosterone (0.5 mg) was injected. After aldosterone injection the peak plasma levels were supraphysiological, reaching nanomolar concentrations. Primary target variables were differences in changes in mean arterial blood pressure, systemic vascular resistance, and cardiac output depending on the pretreatment. Cardiovascular parameters were measured by impedance cardiography during the maintained infusion of the adrenergic modulators for 45 min. Comparing pretreatments, diverse acute, and thus nongenomic, effects of aldosterone on mean arterial blood pressure were observed. After esmolol pretreatment, aldosterone caused an increase in mean arterial blood pressure by 4.1%, whereas after dobutamine pretreatment mean arterial blood pressure decreased by 1.6%, and the difference was statistically significant (P < 0.01). These effects were significant (P < 0.005) for the first 12 min, underlining their nongenomic nature. Our data support the hypothesis that aldosterone, via nongenomic mechanisms, has diverse effects on the cardiovascular system that depend on the preexisting adrenergic state. Furthermore, aldosterone blunts the blood pressure-lowering effect of the beta-blocking agent esmolol by a nongenomic mechanism.

Adrenergic alpha-Agonists↗
PubMed2001

Impact of pharmacotherapy on lymphocyte volumes and activity of the Na+/H+ exchanger in patients with congestive heart failure.

Previous studies in patients with congestive heart failure (CHF) have revealed abnormalities of cellular volume that might have an impact on the dysregulation of peripheral vascular resistance. Human mononuclear leukocytes (HML) represent a model for the study of cellular volume regulation. We investigated the impact of enalapril and carvedilol on HML volume and on the activity of the Na+/H+ exchanger in 26 patients with CHF and 20 volunteers. Over a period of 4 weeks, 18 patients received enalapril in addition to the previous therapy while 8 patients additionally received carvedilol. HML diameters and the activity of the Na+/H+ exchanger were measured by a Coulter Counter. Both patient groups showed abnormally increased initial volumes of HML compared to the volunteer group at baseline. Four weeks of therapy with enalapril in addition to therapy with diuretics and digoxin did not result in a statistically significant reduction of lymphocyte volume, whereas add-on therapy with carvedilol to therapy with ACE inhibitors, diuretics and digoxin reduced the volume significantly. Alterations could not be found in the activity of the Na+/H+ exchanger in either patient group compared to volunteers. Supplementary drug therapy with carvedilol in patients with CHF leads to a reduction of the increased lymphocytic volume, possibly reflecting the beneficial effect of beta-blockade.

Aged↗
PubMed2001

Acute effects of a single oral dose of carvedilol on cardiac sympathovagal balance in man.

Modulation of autonomic activity is considered to be a prognostic marker in patients with cardiovascular disease. The aim of the present study was to evaluate the modulation of sympathovagal balance after single-dose administration of carvedilol using various autonomic tests as challenges of sympathovagal balance. We conducted a randomized double-blind, placebo-controlled study in 18 male volunteers and applied a crossover design. While heart rate variability (HRV) remained unchanged in 24-hour measurements, modulatory effects on sympathovagal balance were demonstrated in controlled autonomic maneuvers at expected maximal drug levels of carvedilol: time-dependent HRV parameters indicative of vagal tone were increased during controlled breathing (15 cycles/min) in the supine body position by carvedilol. The percentage of successive normal RR intervals > 50 ms (pNN50) was increased to 39.8+/-5.1 vs. 32.7+/-4.7% in the placebo group (p < 0.05), root mean square successive differences (rMSSD) to 81.5+/-10.8 vs. 69.3+/-9.1 ms (p < 0.05 vs. placebo). In contrast, carvedilol versus placebo significantly reduced time- and frequency-domain parameters after an active standing-up procedure. This included rMSSD (26.5+/-2.8 ms vs. 34.9+/-3.8 ms), pNN50 (6.9+/-2.2% vs. 12.4+/-2.5%). total power (4329+/-592 ms2 vs. 6428+/-1158 ms2), low frequency (1472+/-179 ms2 vs. 2093+/-284 ms2) and high frequency power (251+/-42 ms2 vs. 353+/-92 ms2) of heart rate variability. Apparently, the effects of even small doses of carvedilol, too low to induce effects detectable in the 24-hour analysis of HRV testing, can be detected on controlled maneuvers of autonomic because of their ability to modulate autonomic balance. Under conditions of vagal stimulation, a potentially beneficial augmentation of HRV parameters indicative for this component is induced by carvedilol, while under conditions of sympathetic activation, carvedilol effects seem opposite. Interpretation of the latter results, in particular, requires further investigation.

Administration, Oral↗
PubMed2001

Improved laboratory confirmation of heparin-induced thrombocytopenia type II. Time course of antibodies and combination of antigen and biologic assays.

We studied whether laboratory confirmation of heparin-induced thrombocytopenia (HIT) can be improved after antigen clearance by determining free antibody and combining the results of an antigenic and a biologic assay. Blood samples taken over 40 days in 14 patients with HIT with thromboembolism underwent fluorescence-linked immunofiltration and the carbon 14-serotonin release assays. Of the 14 patients, 11 showed positive results in both assays at day 1 after stopping heparin. The 3 patients with negative results seroconverted in one or both assays during the subsequent 7 days. Combining the positive results of the assays increased the sensitivity from 85% at day 1 to 100% at day 7. Assay results became negative in all patients within 40 days. The platelet count normalized between days 2 and 9 after withdrawal of heparin. It is assumed that the free antibody can be detected after withdrawal of heparin and after clearance of the platelet factor 4-heparin complex in patients with HIT.

Aged↗
PubMed2000

Rapid, nongenomic steroid actions: A new age?

In the traditional theory of steroid action, steroids bind to intracellular receptors and modulate nuclear transcription after translocation of steroid-receptor complexes into the nucleus. Due to similarities of molecular structure, specific receptors for steroids, vitamin D(3) derivatives, and thyroid hormone are considered to represent a superfamily of steroid receptors. While genomic steroid effects characterized by their delayed onset of action and their sensitivity to blockers of transcription and protein synthesis have been known for several decades, rapid actions of steroids have been more widely recognized and characterized in detail only recently. Rapid effects of steroids, thyroid hormones, and the steroid hormone metabolite of vitamin D(3), 1alpha, 25-dihydroxyvitamin D(3), on cellular signaling and function may be transmitted by specific membrane receptors. Binding sites in membranes have been characterized, exposing binding features compatible with an involvement in rapid steroid signaling. Characteristics of putative membrane receptors are completely distinct from intracellular steroid receptors, a fact which is further supported by the inability of classic steroid receptor antagonists to block nongenomic steroid actions. A putative progesterone membrane receptor has been cloned and functionally expressed with regard to progesterone binding. Development of drugs that specifically affect nongenomic action alone or even both modes of action may find applications in various, areas such as in the cardiovascular and central nervous systems and treatment of preterm labor, infertility, and electrolyte abnormalities.

Animals↗
PubMed2000

Determination of serotonin release from platelets by enzyme immunoassay in the diagnosis of heparin-induced thrombocytopenia.

[14C]-Serotonin release assay (14C-SRA) from platelets is considered to be the most sensitive test for laboratory confirmation of heparin-induced thrombocytopenia (HIT). This study compared 14C-SRA with an enzyme immunoassay (EIA) to determine the release of serotonin from platelets in the presence of heparin and serum from HIT patients. The normal range (median, 2.5 and 97.5 percentiles) of serotonin release from platelets in healthy subjects (n = 149) is 38 ng/ml (19 and 62) measured by EIA-SRA. Serum from HIT patients (n = 42) released 2548 ng/ml (244 and 7987) serotonin in the presence of 0.1 IU/ml heparin and 29 ng/ml (13 and 76) in the presence of 100 IU/ml heparin. One hundred per cent and 15% of HIT samples exhibited an elevated serotonin release from platelets in the presence of 0.1 IU/ml low molecular weight (LMW) heparin, 2100 ng/ml (869 and 5968), or danaparoid, 272 ng/ml (143 and 403), respectively. The sensitivity and specificity of the EIA-SRA was 100% and 97.4% and of the 14C-SRA 100% and 92.9% in HIT patients. No false-positive results were found in patients receiving heparin (n = 28), in patients with elevated levels of bilirubin (n = 5), in patients with antiphospholipid antibody syndrome (n = 10) or in non-HIT patients (n = 78) with both assays. The EIA technique to quantify serotonin release from platelets provides a reliable non-radioactive method to diagnose heparin-induced thrombocytopenia and to assess in vitro crossreactivity of low molecular weight heparins and heparinoid.

Anticoagulants↗
PubMed2000

Specific nongenomic actions of aldosterone.

BACKGROUND: According to the traditional model, steroid hormones modulate gene transcription and protein synthesis. The considerable latency of these genomic steroid effects is the consequence of these time-consuming steps of action. Over the years, it has become increasingly clear that rapid actions of steroids exist that are incompatible with this "classic" genomic model of action. These rapid, nongenomic effects, which recently have been shown for virtually all groups of steroids, are likely to be transmitted by specific membrane receptors. METHODS: A review of data mainly focusing on the nongenomic in vitro and in vivo effects of aldosterone is presented. RESULTS: For rapid aldosterone effects, a prominent example of a receptor/effector cascade for nongenomic steroid effects has been described in various cell types. Nonclassic membrane receptors with a high affinity for aldosterone, but not for cortisol, seem to be involved. As an important second messenger, [Ca2+]i is consistently increased within minutes after the addition of aldosterone. The effects are half maximal at physiological concentrations of free aldosterone (approximately 0.1 nmol/L), while the classic mineralocorticoid antagonist canrenone is ineffective in blocking the action of aldosterone. In addition, cortisol is active only at supramicromolar concentrations. Aldosterone rapidly acts on further cell signaling systems, for example, phosphoinositide hydrolysis and cAMP generation. CONCLUSIONS: For a better understanding of nongenomic aldosterone action even in a clinical context, future research will have to target the cloning of the first membrane receptor for aldosterone and the evaluation of the clinical relevance of rapid steroid effects in general.

Aldosterone↗