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a complex interplay of several factors(passive) is influenced byAldosterone secretion
In addition , sympathetic nerves stimulate beta-1 receptors on granular cells in the kidneyto causerenin secretion
many factors(passive) is influenced byAldosterone secretion
The principal factorsinfluenceglucagon secretion
Control of Glucagon Secretion Two other conditions are knownto triggerglucagon secretion
amino acids , fatty acids , neurotransmitters ( such as adrenaline [ epinephrine ] and gastric inhibitory polypeptide [ GIP ] ) , but a fall in plasma glucose levels(passive) is triggered byGlucagon secretion
hypoglycemia alone(passive) triggered byGlucagon secretion
other factors , including the renin - angiotensin system ( SlOa(passive) to be influenced byaldosterone secretion
Baroreceptors that monitor blood pressurealso influenceADH secretion
various signals involving adrenocorticotropin hormone ( ACTH(passive) is influenced byAldosterone secretion
the adrenocorticotropic hormone ( ACTH ) , natriuretic peptides and certain neurotransmitters(passive) is ... influenced byaldosterone secretion
Negative_regulation ( suppression ) of Localization ( secretion ) of glucagon -conotoxin ) , but not L - type Ca2 + channels ( nifedipinepreventedglucagon secretion
Agonists such as angiotensin II may elevate [ Ca2+]i via multiple mechanisms involving both inhibition of TASK / TREK and Ca2 + release from internal storesto causealdosterone secretion
TTX ) and N - type Ca(2 + ) channels ( omega - conotoxin ) , but not L - type Ca(2 + ) channels ( nifedipinepreventedglucagon secretion
when beta - cell secretion was sufficient but not when beta - cell secretion was deficient(passive) was preventedglucagon secretion
neural inputs from baroreceptors ( which are located in the carotid sinus , aoric arch and atrium(passive) is triggered byThe ADH secretion
Downstream of the KATP channel , inhibition of voltage - gated Na+ ( TTX ) and N - type Ca2 + channels ( ω - conotoxin ) , but not L - type Ca2 + channels ( nifedipinepreventedglucagon secretion
Downstream of the K - ATP channel , inhibition of voltage - gated Na+ ( TTX ) and N - type Ca2 + channels ( omega - conotoxin ) , but not L - type Ca2 + channels ( nifedipinepreventedglucagon secretion
Loss of blood pressure or nausea and vomitingcan ... triggerADH secretions
diminished flowcausesaldosterone secretion
the PLD - generated DAGcan triggeraldosterone secretion
■ Severe volume depletionleadingto ADH secretion
sodium depletion(passive) caused byaldosterone secretion
High doses of heparincan preventaldosterone secretion
a decrease in blood pressure or blood volume , or a decrease in sodium levels of the blood(passive) is triggered byAldosterone secretion
the simultaneous actions of AngII and corticotrophin ( Spät and Hunyady , 2004(passive) is triggered byaldosterone secretion
failure of the action of angiotensinto causealdosterone secretion
low salt levels(passive) is triggered byAldosterone secretion
A reduction of around 8 - 10 % of body volume of waterwill resultin ADH secretion
Stimulation of β -adrenoceptors in renal1 835 juxtaglomerular cells by the sympathetic postganglionic neuronscausesrenin secretion
a stimuluscausesrenin secretion
Similar drugs function as AT II receptor antagoniststo preventaldosterone secretion
increases in renal perfusion pressure(passive) caused byrenin secretion
PTH - rp secretion(passive) Caused byADH secretion Hypercalcemia
excessive potassium in the blood(passive) is also triggered byAldosterone secretion
adenosine , 2-chloroadenosine ( 1.65 C 10(-6(passive) provoked byglucagon secretion
a new and unexpected pathwaymay influencerenin secretion
bladder distention 14(passive) can be influenced byADH secretion
Ang II , adrenocorticotropic hormone , and potassium.32(passive) is influenced byAldosterone secretion
the loss of cell - cell contacts(passive) triggered byglucagon secretion
in less sodium and water retentionresultsin less sodium and water retention
peripheral vasoconstriction and water retentioncausesperipheral vasoconstriction and water retention
water reabsorption in the nephronto preventwater reabsorption in the nephron
to Na+ reabsorption and water retention stimulates production of RBCleadsto Na+ reabsorption and water retention stimulates production of RBC
Na and Water retention Fluid is lost in the interstitial spacescausesNa and Water retention Fluid is lost in the interstitial spaces
in excess sodium and fluid retentionresultingin excess sodium and fluid retention
to the development of SIADHledto the development of SIADH
to increased water reabsorption and increasingly concentrated urineleadsto increased water reabsorption and increasingly concentrated urine
excessive free water retention that creates a moderate effect ( < 10 % ) in intravascular volumecreatesexcessive free water retention that creates a moderate effect ( < 10 % ) in intravascular volume
secondary aldosterone secretion , renal tubular sodium and water reabsorption factors increasecausingsecondary aldosterone secretion , renal tubular sodium and water reabsorption factors increase
in increased systemic blood pressure [ 15resultingin increased systemic blood pressure [ 15
in an overall improvement in the glucose homoeostasis.1 Treatment with linagliptinthus resultingin an overall improvement in the glucose homoeostasis.1 Treatment with linagliptin
in better regulation of glucose homeostasisthus resultingin better regulation of glucose homeostasis
from low - frequency renal nerve stimulation ( 0.5 Hzresultingfrom low - frequency renal nerve stimulation ( 0.5 Hz
in an overall improvement in the glucose homoeostasis.2 Insulin add - on therapythus resultingin an overall improvement in the glucose homoeostasis.2 Insulin add - on therapy
in excess sodium malesresultingin excess sodium males
in an overall improvement in the glucose homoeostasis.1 Linagliptin ( 5 mg , once - dailythus resultingin an overall improvement in the glucose homoeostasis.1 Linagliptin ( 5 mg , once - daily
in an overall improvement in the glucose homeostasisthus resultingin an overall improvement in the glucose homeostasis
to reduced hepatic glucose output.7 Hindrances in delivery of GLP-1leadsto reduced hepatic glucose output.7 Hindrances in delivery of GLP-1
to an increase in serum potassium with simultaneous removal of sodium and fluidcan leadto an increase in serum potassium with simultaneous removal of sodium and fluid
to retention of Na and fluid-- >Leadsto retention of Na and fluid-- >
retention of Na+ and Watercausesretention of Na+ and Water
in increased production of glucose by the liver ( 19resultingin increased production of glucose by the liver ( 19
in excess sodium highest among recreational sportspeopleresultingin excess sodium highest among recreational sportspeople
the kidneys to reabsorb more Na+ and watercausingthe kidneys to reabsorb more Na+ and water
formation of angiotensin 2.Angiotnesin 2 causes generalised vasoconstriction and increased release of aldosteronecausesformation of angiotensin 2.Angiotnesin 2 causes generalised vasoconstriction and increased release of aldosterone
in increased production of glucose by the liver To prove an association between AVP and glucose , Hsu et alresultingin increased production of glucose by the liver To prove an association between AVP and glucose , Hsu et al
increased water and salt retention in kidneys resting SBP above 140 or DBP above 90usually due to kidneys not secreting enough salt and watercausingincreased water and salt retention in kidneys resting SBP above 140 or DBP above 90usually due to kidneys not secreting enough salt and water
to aldosterone secretion and Na+ reabsorption and thus , increases body fluid volume and pressureleadsto aldosterone secretion and Na+ reabsorption and thus , increases body fluid volume and pressure
to high - pressure voiding that causes the sphere is so much at atomic length scales that it consists of propagating wave frontsleadsto high - pressure voiding that causes the sphere is so much at atomic length scales that it consists of propagating wave fronts
sodium retention , an increase in blood pressure , and restoration of renal perfusion , which shuts off the signal for renin release ( negative feedbackcausessodium retention , an increase in blood pressure , and restoration of renal perfusion , which shuts off the signal for renin release ( negative feedback
in increased blood volume.aresultsin increased blood volume.a
the angiotensin conversioncausesthe angiotensin conversion
to plasma expansion and increased perfusionleadingto plasma expansion and increased perfusion
sodium retention , which then prevents excretion of sodium bicarbonatecausessodium retention , which then prevents excretion of sodium bicarbonate
in retention of free waterresultingin retention of free water
waterr retention andcausingwaterr retention and
to sodium retention , an increase in circulation blood volume , and a rise in blood pressureleadsto sodium retention , an increase in circulation blood volume , and a rise in blood pressure
maximal sodium conservation by the tubules and the ratio is less than 1 %causesmaximal sodium conservation by the tubules and the ratio is less than 1 %
an increase in fluid retention 1.5causesan increase in fluid retention 1.5