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PubMed1979

Short-latency drinking and increased Na appetite after intracerebral microinjections of NGF in rats.

NERVE GROWTH FACTOR (NGF) is a polypeptide trophic factor for peripheral sympathetic and sensory neurones(1,2). Apparent NGF(3-5) and NGF receptors(6,7) have also been identified in the brain, and intracerebral administration of NGF in the adult rat produces marked biochemical(8) and morphologica(9,10) changes in brain tissue. These findings, taken together with the observations that central injections of NGF facilitate behavioural recovery from brain damage(11,12), indicate that this polypeptide may have an important role in brain function. It has been observed that rats given intraventricular injections of up to 2.3 microg NGF drink copiously (M.E.L. and G. Guroff, unpublished observations). Perkins et al.(13) reported that diencephalic application of crystalline NGF (1-15 microg) resulted in an intense polydipsia. The present report confirms the observations of M.E.L. and Guroff, and extends the findings of Perkins et al.(13) by using solutions of NGF instead of crystals. It also describes for the first time a second phenomenon produced by intracranial administration of NGF, namely an intense appetite for aversive concentrations of sodium solutions.

Journal Article↗

PubMed1979

Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin.

Angiotensin II is dipsogenic, and vasopressin (ADH) regulates renal water excretion. Together, these hormones govern overall mammalian water balance. The Brattleboro rat with inherited diabetes insipidus (DI) lacks ADH and is therefore a convenient model with which to elucidate mechanisms regulating water metabolism. In the present studies, angiotensin II has also been removed from DI rats by the administration of an inhibitor (captopril, SQ 14225; D-2-methyl-3-mercaptopropanoyl-L-proline) of the enzyme which converts angiotensin I, the relatively inert component of the renin-angiotensin system, to angiotensin II, the biologically active substance. SQ 14225 reduced the drinking rates, and after 6 days lowered peripheral plasma aldosterone concentrations were associated with hyperkalaemia. We conclude that the polydipsia of diabetes insipidus partly results from elevated plasma renin activities and angiotensin II concentrations seen in this syndrome. Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting.

Adrenal Cortex Hormones↗

PubMed1995

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis.

Very few patients with familial hypomagnesemia, hypercalciuria and nephrocalcinosis have been described. Information about clinical course, familial studies or evolution after renal transplantation is very scant. We have studied eight patients with this syndrome who belong to five different families. The mean age at diagnosis was 15 +/- 7 years (5 to 25 years). The primary clinical data were polyuria-polydipsia (8 cases), ocular abnormalities (5), recurrent urinary tract infections (5) and recurrent renal colics with stone passage (2). Bilateral nephrocalcinosis was observed in all cases. Every patient showed hypomagnesemia (1.1 +/- 0.2 mg/dl) with inappropriately high urinary magnesium (Mg) excretions (70 +/- 17 mg/day), Mg clearances (4.4 +/- 1.2 ml/m) and Mg fractional excretions (16.2 +/- 7.1%). Hypercalciuria was present in every case except in those with advanced renal insufficiency. Serum parathormone levels were abnormally high. Serum calcium (Ca), phosphorus and potassium, and urinary excretions of uric acid and oxalate were normal. Neither chronic oral Mg administration nor thiazide diuretics normalized serum Mg levels or urinary Ca excretions, respectively. Follow-up was 6 +/- 4.5 years. Renal function worsened in every case with six patients starting on chronic dialysis after 4.3 +/- 3.8 years. The progression rate of renal insufficiency correlated with the severity of nephrocalcinosis. Five patients have received a kidney graft, and their serum Mg and urinary Ca have always been within normal values after transplantation. Twenty-six members of four of the affected families were studied: none of them showed hypomagnesemia, renal insufficiency or nephrocalcinosis. However, eleven cases (42%) had hypercalciuria and four of them presented with recurrent renal stones. Two family members had medullary sponge kidneys. In conclusion, progression to renal insufficiency is common in this syndrome; oral Mg and thiazide diuretics are ineffective to correct abnormalities. After kidney graft, tubular handling of Mg and Ca was normal. A striking incidence (42%) of hypercalciuria was found in the familial study.

Adolescent↗

PubMed2006

Cushing's syndrome caused by an occult source: difficulties in diagnosis and management.

BACKGROUND: A 24-year-old woman presented with a 12.5 kg weight gain over 6 months (mostly abdominal), hirsutism, acne, ankle edema, polydipsia, nocturia, back pain, pigmentation, poor libido and lightened menses to our hospital in May 1986. She had been treated for the previous 2 years with furosemide and spironolactone for peripheral edema, and had stopped the combined oral contraceptive 2 months previously. She did not take tobacco, recreational drugs or alcohol. Upon physical examination she was grossly Cushingoid with florid clinical manifestations. INVESTIGATIONS: Serum potassium and bicarbonate, circadian rhythm of cortisol, low-dose and high-dose dexamethasone suppression tests, plasma adrenocorticotropic hormone (ACTH), corticotropin releasing-hormone stimulation test, CT scan of the pituitary, plain chest radiology, CT scan of the chest and abdomen, trans-sphenoidal pituitary biopsy and histology, CT scan and MRI of the thorax, MRI of the pituitary, octreotide scintigraphy, gastroscopy, colonoscopy, gut peptides, tumor markers, urine 5-hydroxyl-indole-acetic acid, resection, histology, immunocytochemistry and in situ hybridization. DIAGNOSIS: Occult ectopic ACTH syndrome from a presumed appendiceal neuroendocrine tumor. The tumor was only identified some 20 years from initial presentation. MANAGEMENT: Adrenolytic therapy before bilateral adrenalectomy to cure Cushing's syndrome, glucocorticoid and mineralocorticoid replacement therapy, and then repeated surveillance over 20 years to locate the ectopic source of ACTH. This was finally identified by CT scan and excised at laparotomy.

ACTH Syndrome, Ectopic↗

PubMed2005

Clinical presentation of type 2 diabetes mellitus in children and adolescents.

OBJECTIVE: Recent reports indicate an increasing prevalence of type 2 diabetes mellitus (TD2M) in children and adolescents around the world in all ethnicities, possibly due to increasing prevalence of obesity. Therefore, it is essential that clinicians are aware of the clinical features of T2DM in these age groups. METHODS: All published cases of T2DM in children and adolescents were evaluated and the different clinical presentations of T2DM in minorities and Caucasian described. RESULTS: Manifestation of T2DM is usually at mid-to-late puberty with few symptoms such as mild-polyuria or polydipsia. Most of the children and adolescents are extremely obese. The great majority of children and adolescents with T2DM have relatives with T2DM, and show other clinical features of the insulin resistance syndrome such as hypertension, dyslipidemia, polycystic ovarian syndrome (PCOS) or acanthosis nigricans. One-third of the minority children with T2DM and the majority of the Caucasian children with T2DM were detected by screening in the absence of symptoms. CONCLUSIONS: It is becoming increasingly clear that overweight children above the age of 10 y with (1) clinical signs of insulin resistance (acanthosis nigricans, dyslipidemia, hypertension, PCOS), or (2) relatives with T2DM, or (3) of particular ethnic populations (Asian, Indians, Africa-Americans, Hispanics), or (4) extremely obese children should be screened for T2DM.

Adolescent↗

PubMed2005

Decreased expression of AQP2 and AQP4 water channels and Na,K-ATPase in kidney collecting duct in AQP3 null mice.

BACKGROUND INFORMATION: Phenotype analysis has demonstrated that AQP3 (aquaporin 3) null mice are polyuric and manifest a urinary concentration defect. In the present study, we report that deletion of AQP3 is also associated with an increased urinary sodium excretion. To investigate further the mechanism of the decreased urinary concentration and significant natriuresis, we examined the segmental and subcellular localization of collecting duct AQPs [AQP2, p-AQP2 (phosphorylated AQP2), AQP3 and AQP4], ENaC (epithelial sodium channel) subunits and Na,K-ATPase by immunoperoxidase and immunofluorescence microscopy in AQP3 null (-/-), heterozygous (+/-) mice, wild-type and unrelated strain of normal mice. RESULTS: The present study confirms that AQP3 null mice exhibit severe polyuria and polydipsia and demonstrated that they exhibit increased urinary sodium excretion. In AQP3 null mice, there is a marked down-regulation of AQP2 and p-AQP2 both in CNT (connecting tubule) and CCD (cortical collecting duct). Moreover, AQP4 is virtually absent from CNT and CCD in AQP3 null mice. Basolateral AQP2 was virtually absent from AQP3 null mice and normal mice in contrast with rat. Thus the above results demonstrate that no basolateral AQPs are expressed in CNT and CCD of AQP3 null mice. However, in the medullary-collecting ducts, there is no difference in the expression levels and subcellular localization of AQP2, p-AQP2 and AQP4 between AQP3 +/- and AQP3 null mice. Moreover, a striking decrease in the immunolabelling of the alpha1 subunit of Na,K-ATPase was observed in CCD in AQP3 null mice, whereas a medullary-collecting duct exhibited normal labelling. Immunolabelling of all the ENaC subunits in the collecting duct was comparable between the two groups. CONCLUSIONS: The results improve the possibility that the severe urinary concentrating defect in AQP3 null mice may in part be caused by the decreased expression of AQP2, p-AQP2 and AQP4 in CNT and CCD, whereas the increased urinary sodium excretion may in part be accounted for by Na,K-ATPase in CCD in AQP3 null mice.

Animals↗

PubMed1977

The effect of chronic diabetes, induced by streptozotocin, on the activities of some enzymes of glycerolipid synthesis in rat liver.

1. Rats were injected with a single dose of 35mg of streptozotocin/kg body wt. They exhibited a diabetes that was characterized by glycosuria, polyuria, polydipsia, hyperphagia, hyperglycaemia, increased concentrations of unesterified fatty acids, glycerol and triacylglycerols in the serum and an increased activity of glucose 6-phosphatase in the liver. 2. After 10 weeks the hepatic activities of the microsomal glycerol phosphate acyltransferase, phosphatidate phosphohydrolase, phosphatidate cytidylyltransferase, diacylglycerol acyltransferase, choline phosphotransferase, CDP-diacylglycerol--inositol phosphatidyltransferase and the soluble phosphatidate phosphohydrolase were measured. 3. The only significant changes were an increase in the activity of the soluble phosphatidate phosphohydrolase and a decrease in that of the CDP-diacylglycerol--inositol phosphatidyltransferase in the diabetic rats. 4. These results are discussed in relation to the control of glycerolipid synthesis.

Acyltransferases↗

PubMed1976

Deoxycorticosterone hypertension in the pig.

1. Deoxycorticosterone acetate (DOCA) implantation (100 mg/kg) caused mean arterial pressure to rise in 5-10 days from control pressures of 100-115 mmHg to stable hypertensive values of 140-160 mmHg in approximately 1 month. In six of seven pigs elevations of mean arterial pressure were entirely the result of increased total peripheral resistance. 2. Single implants maintained serum DOCA at approximately ten times normal concentration for up to 90 days. 3. Moderate but variable decreases in serum aldosterone followed implantation. 4. Hypokalaemia, polydipsia and suppressed plasma renin activity were evident by the fifth post-implantation day and persisted thereafter. No consistent change occurred in serum sodium. 5. Noradrenaline or angiotensin caused increases in total peripheral resistance at lower threshold infusion rates in hypertensive pigs compared with control animals. 6. In isolated, perfused hind-limb preparations, hypertensive vascular beds were characterized by both functional (increased vascular smooth muscle sensitivity) and structural (elevated resistance of maximally dilated vascular bed) changes. 'Protection' from increased arterial wall stresses in hypertensive pigs prevented structural, but not functional, alterations.

Angiotensin II↗

PubMed1984

The antihypertensive effect of dietary potassium chloride loading in rats with adrenal regeneration hypertension.

Adrenal regeneration hypertension was induced in male Wistar rats by unilateral adrenal enucleation, contralateral adrenalectomy and the provision of a 1% (w/v) NaCl solution for drinking. A fivefold increase in dietary KCl content caused a significant reduction in the systolic blood pressure of hypertensive rats but not of control rats. During the increase in potassium intake there was a marked polydipsia. When 1% NaCl solution was the drinking fluid, the resultant increase in sodium intake was associated with an abolition of the antihypertensive effect of potassium loading, but when the sodium intake was held constant, the antihypertensive effect was maintained. In rats with adrenal regeneration hypertension, plasma volume was significantly higher, and packed cell volume and plasma protein concentrations were significantly lower than in control rats. These differences were abolished after 4 days of dietary KCl supplementation. Increased dietary potassium intake was associated with significantly lower serum aldosterone concentrations and significantly higher plasma potassium concentrations in adrenal enucleated rats compared with controls. The possibility that a reduction in extracellular fluid volume (due to a natriuresis) and/or a peripheral vasodilatation contributed to the antihypertensive effect of KCl loading is discussed.

Adrenal Glands↗

PubMed1993

Chronic insulin treatment in rats: evidence against a role for insulin as a pressor agent.

1. The present study was undertaken to test whether insulin acts as a pressor agent and causes hypertension in rats. 2. Insulin at doses of 10 or 100 units day-1 kg-1 was administered daily by subcutaneous injection to normal rats for 6 weeks. As it has been suggested that sodium retention plays a major role in the putative hypertensive activity of this hormone, insulin was also administered to saline- (1% NaCl) drinking rats according to the same protocol. Water- and saline-drinking rats served as controls. 3. After 6 weeks of insulin treatment, the mean arterial blood pressure did not increase in any of the insulin-treated or the insulin-salt-treated groups. However, in both insulin-salt-treated groups, absolute and relative ventricular and renal hypertrophy with increased ventricular water content as well as increased urine output with reduced osmolality were observed. 4. All insulin-treated groups showed increased plasma levels of glucose, insulin and antidiuretic hormone when compared with their respective controls. 5. These results demonstrate that chronic insulin treatment did not increase blood pressure in rats, even when drinking water was supplemented with NaCl, and suggest that a polyuria-polydipsia syndrome was present in both insulin-salt-treated groups. Moreover, increased plasma levels of antidiuretic hormone were observed in all insulin-treated groups.

Animals↗

PubMed1996

Apparent mineralocorticoid excess due to 11 beta-hydroxysteroid dehydrogenase deficiency: a possible cause of intrauterine growth retardation.

A Japanese boy with apparent mineralocorticoid excess (AME) is described. He was born with intrauterine growth retardation (IUGR) and elevated serum level of creatine phosphokinase (CPK). He was studied at 2 years of age because of polyurea and polydipsia of one year's duration and was found to have hypokalaemic alkalosis and sustained hypertension. His plasma renin activity and aldosterone levels were always low and his ratio of urinary tetrahydrocortisol plus allo-tetrahydrocortisol to that of tetrahydrocortisone was very high. Therefore, AME due to 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) deficiency was diagnosed. He was successfully treated with a combination of spironolactone and nifedipine for at least 16 months. His blood pressure, plasma pH and serum potassium levels were normalized by this treatment, but serum CPK level remained high. We researched the birth records of previously reported AME cases and found that IUGR is a characteristic feature of AME. The mechanism by which IUGR occurs in AME is discussed and we speculate that 11 beta-HSD might be deficient in the placenta and/or fetal tissues, as well as in the kidney, in AME. An explanation for the elevated CPK could not be found.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed2000

Vasopressin and thirst in patients with posterior pituitary ectopia and hypopituitarism.

OBJECTIVE: Partial diabetes insipidus has been documented in patients with congenital hypopituitarism and posterior pituitary ectopia, some cases being clinically silent except for enuresis. The objective of our study was to evaluate vasopressin (AVP) secretion and thirst appreciation in hypopituitary patients with posterior pituitary ectopia. PATIENTS: Twelve males and three females, aged between 13 and 38 years (median 19 years). Eleven had multiple pituitary deficiencies, adequately replaced at the time of the study, and four were only growth hormone deficient. None of the patients suffered from polyuria, polydipsia or nocturnal enuresis. We tested the patients with a 5% NaCl infusion. Five patients with abnormal vasopressin production were also tested with nitroprusside, which affects baroceptor vasopressin secretion. RESULTS: We found that only two out of 12 patients had normal AVP secretion. Thirst assessment showed severe hypodipsia in one patient, hyperdipsia in three out of 15 and more subtle abnormalities in two out of 15 patients. Concordance was found between osmotically and baroceptor-stimulated vasopressin. CONCLUSIONS: Patients with posterior pituitary ectopia showed a high prevalence of subclinical subnormal vasopressin response to the osmolar stimulus and moreover an impairment of thirst appreciation. Our data on nonosmotically stimulated AVP release suggest the existence of a damage in the hypothalamic vasopressin secreting centres.

Adolescent↗

PubMed1998

Recovery from Marie-Bamberger's syndrome and diabetes insipidus after removal of a lung adenocarcinoma with neuroendocrine features.

A 44-year-old woman with Marie-Bamberger's syndrome and diabetes insipidus had a lung tumour with mediastinal metastases, but no signs of metastases to the hypothalamus or pituitary gland. A week after removal of the tumour, the joint pain, polyuria and polydipsia disappeared. The tumour was diagnosed histopathologically as a moderately differentiated adenocarcinoma with focal neuroendocrine cell differentiation and dispersed cells reacting with antisera against neurone-specific enolase, S-100 protein, neuropeptide Y, follicle-stimulating hormone, substance P, vasoactive polypeptide (VIP), adrenocorticotropic hormone and pancreatic polypeptide (PP) as well as to one of three tested antisera raised against antidiuretic hormone (ADH). It was suggested that Marie-Bamberger's syndrome might be caused by one of these immunoreactive substances or by a substance that shares an amino acid sequence with one of these neuroendocrine peptides. It was also suggested that the tumour might produce an ADH-like substance which might have an ADH-antagonist effect.

Adenocarcinoma↗

PubMed2001

Hypercalcaemia of malignancy: an undiagnosed and undertreated disease.

BACKGROUND: Hypercalcaemia of malignancy, a relatively frequent phenomenon, seems to be insufficiently recognized and treated. Its symptoms are not specific, but they affect the quality of life. METHODS: A prospective study to analyse the influence of symptoms caused by hypercalcaemia on the decision of the admitting physician, the motivation for treatment, and the effect of the treatment on the given symptoms in hospitalized patients with oncologic disease in progression, where confounding causes of similar symptoms such as cerebral metastasis, radiotherapy, treatment with opioids, etc., were excluded. RESULTS: A total of 71 patients, mean age 65 + 11 years, fulfilled the strict inclusion criteria. About 42% were hospitalized because of symptoms caused by hypercalcaemia, but none of the medical reports mentioned hypercalcaemia as reason for hospitalization. Specific antihypercalcaemic therapy was given to only 37% of patients, and only 25% got an adequate rehydratation. Antihypercalcaemic treatment was guided by the severity of hypercalcaemia (>3.00 mmol L(-1)), not by the symptoms. Polyuria-polydipsia, nausea-vomiting and constipation were correlated with hypercalcaemia. These symptoms, as well as confusion-stupor and bone pains improved significantly when calcaemia was normalized. Patients with calcaemia normalized returned home most frequently (P < 0.03). CONCLUSIONS: Malignant hypercalcaemia remains mostly undiagnosed in medical praxis. Specific treatment occurs in too small fractions of the patients. As the normalization of calcaemia significantly improves the symptoms because of hypercalcaemia and the quality of life, rapid rehydration and specific calcium lowering treatments should be part of palliative measures in all patients with malignant hypercalcaemia.

Bone and Bones↗

PubMed1996

Osmoregulation of plasma vasopressin in diabetes mellitus with sustained hyperglycemia.

We studied osmoregulation of plasma vasopressin in 5 patients with newly diagnosed diabetes mellitus. All patients showed typical symptoms of uncontrolled diabetes mellitus such as marked hyperglycemia, polyuria, and polydipsia, but did not have advanced diabetic complications. Vasopressin release was studied using 5% hypertonic saline infusion test twice: before treatment when the patient was hyperglycemic, and after treatment 1 to 2 months later when the patient was euglycemic. Plasma vasopressin was measured by a sensitive and specific radioimmunoassay. The mean basal plasma vasopressin value in the patients was significantly higher in the hyperglycemic compared with the euglycemic state (3.75 +/- 0.70 vs 1.18 +/- 0.46 pmol/l, respectively; P < 0.05). The relationship of plasma vasopressin with serum sodium, but not plasma osmolality, during hyperglycemia showed an apparent hypersecretion of vasopressin. In both cases, the sensitivity of the vasopressin response to osmotic stimuli was significantly decreased. During euglycemia, the sensitivity of vasopressin secretion to either sodium or osmolality was almost normal, although a slight rise in the osmostat was observed compared with normal subjects. Together, we found that the positive correlation of vasopressin with sodium or osmolality is maintained but significantly altered in patients with untreated diabetes mellitus. Especially noteworthy is the lowered threshold and decreased sensitivity of osmotically-induced vasopressin secretion during hyperglycemia, which may be caused by multiple factors such as diabetes-associated hypovolemia, osmogenic effects of glucose and other osmoles, depletion of the pool of vasopressin available for release, and the metabolic derangement of osmoreceptor/magnocellular neurons.

Adult↗

PubMed2001

Evaluation of the clinical efficacy of marbofloxacin (Zeniquin) tablets for the treatment of canine pyoderma: an open clinical trial.

The efficacy and field safety of marbofloxacin (Zeniquin) for the treatment of superficial and deep bacterial pyoderma were evaluated. Seventy-two dogs were treated with 2.75 mg kg-1 of marbofloxacin orally once daily for 21 or 28 days. Sixty-two dogs (86%) had superficial pyoderma and 10 (14%) had deep pyoderma. A history of prior pyoderma was reported in 39/72 dogs. Pretreatment aerobic bacteriologic cultures of skin lesions were performed in 47 cases and the predominant pathogen isolated was Staphylococcus intermedius. Treatment was successful in 62/72 (86.1%) dogs, improvement was noted in 6/72 (8.3%) dogs and treatment failed in 4/72 (5.6%) dogs. Adverse effects associated with treatment included listlessness, anorexia, vomiting, soft stool, flatulence and polydipsia; these adverse effects were seen in only 6/81 dogs. Marbofloxacin was safe and effective for the treatment of superficial and deep pyoderma in dogs at the dosage used in this study.

Administration, Oral↗

PubMed2003

Rare association of xanthoma disseminatum with skeletal involvement.

A ten-year-old boy presented with a 2.5-year history of painful shoulder and hip joints, 1.5 years of yellow-brown papules and plaques on the face, flexures and trunk, and 6 months of polyuria and polydipsia. Skin biopsy revealed histological and immunohistochemical features typical of xanthoma disseminatum. Lytic bone lesions were seen in the femur and pelvis and sclerotic changes in the humerus on X-ray. Diabetes insipidus was also diagnosed

Biopsy↗

PubMed2001

Renal phenotype of low kallikrein rats.

BACKGROUND: Renal kallikrein has been linked with inheritance of arterial hypertension and with sensitivity to drug nephrotoxicity. Identification of a cause--effect relationship between low kallikrein and intermediate phenotypes has been hampered by the lack of adequate animal models. METHODS: Kallikrein was measured in tissues obtained from rats inbred for low urinary kallikrein excretion (LKR) and wild-type controls. Blood pressure and indices of myocardial contractility were recorded via an intraventricular cannula connected to a transducer. The functional relevance of endogenous angiotensin II (Ang II) in LKR was explored by determining the effect of Ang II subtype 1 (AT(1)) receptor blockade on glomerular filtration rate, renal blood flow, and urinary sodium excretion. In addition, sensitivity to gentamycin-induced nephrotoxicity was evaluated. RESULTS: Kallikrein activity was reduced by 60% in the kidney of LKR (P < 0.01), whereas it was increased in the heart (P < 0.05) and was unaltered in the pancreas, liver, and salivary glands. Heart rate and myocardial contractility were reduced, and the mean blood pressure (MBP) was increased in LKR as compared with controls (P < 0.05). LKR exhibited polydipsia, polyuria, glomerular hyperfiltration, and reduced fractional sodium excretion under basal conditions and impaired renal vasodilation in response to volume expansion. These functional alterations were significantly attenuated by AT(1) receptor blockade. Gentamycin reduced the glomerular filtration rate in LKR, but not in controls. CONCLUSIONS: In LKR, unopposed activity of Ang II appears to be responsible for increased glomerular hydrostatic pressure and augmented tubular reabsorption. Balance between the kallikrein-kinin and renin-angiotensin systems is essential for normal renal function.

Angiotensin Receptor Antagonists↗