Familial neurohypophyseal diabetes insipidus is a disease caused by a mutation in the gene encoding antidiuretic hormone (ADH), leading to a change in its amino acid sequence. This change prevents ADH from binding to its receptor.

Explain why this change prevents ADH binding to its receptor.

Figure 1 shows the intracellular pathway in collecting duct cells that regulates water reabsorption.

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A drug that inhibits the activity of Adenylate Cyclase (AC) can cause nephrogenic diabetes insipidus, resulting in the excretion of a high volume of dilute urine.

Use Figure 1 to explain why.

Renal glycosuria is a condition where glucose is excreted in the urine, even though blood glucose levels are normal. It is caused by a mutation in the gene for SGLT2 sodium-glucose co-transport proteins.

Using your knowledge of the kidney, explain why glucose is found in the urine of a person with renal glycosuria.

Evaluate this conclusion.

Describe and explain how three structural features of the epithelial cells lining the proximal convoluted tubule (PCT) adapt them for the rapid reabsorption of glucose from the glomerular filtrate.

Identify the two regions of the renal tubule where ADH stimulates the insertion of aquaporins into the luminal membranes of the epithelial cells.

Aquaporins are highly selective channel proteins that allow the passage of water but prevent the passage of hydronium ions ($H_3{O}^{+}$). Suggest and explain how the structure of an aquaporin ensures this selectivity.

A decrease in the solute concentration (osmolarity) of blood plasma (such as after drinking a large volume of water) causes a reduction in ADH secretion. State the precise location of the receptors that detect this change, and explain how the resulting reduction in ADH release restores the solute concentration of the blood plasma to its normal range.

Calculate the difference in the number of volunteers between the two groups who achieved target glycemic control. Show your working.

In desert rodents, efficient reabsorption of essential solutes such as glucose from the glomerular filtrate is vital to prevent metabolic waste. Describe and explain three structural adaptations of epithelial cells lining the proximal convoluted tubule that facilitate the rapid selective reabsorption of glucose into the blood.

The drug Tolvaptan is a selective antagonist that blocks ADH (vasopressin) receptors, preventing the insertion of aquaporins. Name the two regions of the tubule system in a nephron where this drug directly prevents water reabsorption.

Aquaporins are highly selective, allowing only polar water molecules ($H_{2}O$) to pass through while completely blocking other small ions like protons ($H^{+}$). Suggest and explain how the structure of the aquaporin channel achieves this selectivity.

A patient suffering from head trauma experiences a condition where the secretion of ADH in response to high blood solute concentration (high plasma osmolarity) is severely impaired. State the precise location of the sensory receptors that normally detect an increase in blood solute concentration, and explain how this impairment in ADH release affects the solute concentration of both the patient's urine and their blood plasma.

Type 1 congenital nephrogenic diabetes insipidus is a rare genetic disorder caused by a mutation in the AVPR2 gene. This gene encodes the V2 receptor (a G-protein coupled receptor) located on the basolateral membrane of kidney collecting duct cells. The mutation changes the amino acid sequence of the V2 receptor, preventing antidiuretic hormone (ADH) from binding to it.

Explain why this change prevents ADH binding to the receptor.

Figure 1 shows the intracellular pathway in collecting duct cells that regulates water reabsorption.

Draw on this

A drug known as H-89 acts as a selective inhibitor of Protein Kinase A (PKA). Patients taking this drug can develop temporary nephrogenic diabetes insipidus, resulting in the excretion of a high volume of dilute urine.

Use Figure 1 to explain why.

Renal phosphaturia is a disorder characterised by the excretion of abnormally high levels of phosphate in the urine, even when blood phosphate concentrations are within the normal range. This condition is caused by a loss-of-function mutation in the gene encoding the NaPi-IIa sodium-phosphate co-transport protein.

Using your knowledge of the kidney, explain why phosphate is found in abnormally high levels in the urine of a person with renal phosphaturia.

Using information from the figure, explain how the secretion of pro-NTX is controlled by positive feedback.

Elevated local temperatures during neuroinflammation cause the inactive protein pro-NTX to change into its active form, NTX. Suggest how.

The binding of GS-A to astrocyte receptors leads to a significant increase in the rate of aerobic respiration in these cells. Explain how.

Explain how a longer loop of Henle in the desert hopping mouse (Notomys alexis) enables it to survive in extremely arid conditions with very limited access to drinking water.

Ecophysiologists studying water-conservation adaptations in arid-zone mammals model the relationship between the maximum urine concentration, $U$ (in ${mOsmol\; kg}^{-1}$), and the relative medullary thickness, $M$, using the equation: $U=380(M-0.4)+372$ Calculate the relative medullary thickness of a species of hopping mouse that produces a maximum urine concentration of $3830{mOsmol\; kg}^{-1}$. Show your working.

Name the region of the brain containing osmoreceptors that detect changes in blood water potential.

MDMA (ecstasy) stimulates the secretion of excess ADH into the blood. Suggest two physiological changes or signs that may result from this increase in ADH.

Describe the cellular mechanism by which ADH increases the reabsorption of water in the collecting ducts of the kidneys.