Physiology
Renal
In tubuloglomerular feedback, where is increased tubular flow rate detected in the nephron:
Answer:
Methods of autoregulation:- The myogenic mechanism: where an increase in intravascular pressure stimulates stretch receptors in the vessel wall causing a reflex smooth muscle contraction and hence vessel vasoconstriction and reduced flow.
- The tubuloglomerular feedback mechanism: where an increase in tubular flow rate (with a resultant increase in tubular NaCl concentration detected by the macula densa) causes the juxtaglomerular apparatus to release adenosine which produces afferent arteriolar vasoconstriction and reduces GFR.
Renal Blood Supply
Physiology / Renal / Functional Anatomy
Last Updated: 26th July 2024
The kidneys receive about 20% of total cardiac output ( ~1 L/min).
Functional Anatomy
The renal artery enters via the hilus and divides into two or three segmental arteries which further divide into interlobar arteries running between the renal pyramids to the corticomedullary border, where they split into arcuate arteries. The arcuate arteries curve parallel to the outer surface of the kidney and give rise to the interlobular arteries which ascend into the cortex and feed the afferent arterioles of the glomerulus. The capillaries of the glomerulus are the site of filtration, and drain into the efferent arteriole. Afferent and efferent arterioles provide the major resistance to renal blood flow.
In the outer two-thirds of the cortex, the efferent arterioles branch into a network of peritubular capillaries which supply all cortical parts of the nephrons. Capillaries close the corticomedullary border in the inner third of the cortex, loop into the medulla to form the vasa recta surrounding the loop of Henle. The vasa recta and peritubular capillaries drain into the renal veins.
Structural Arrangement of the Renal Blood Supply. (Image by OpenStax College [CC BY 3.0 , via Wikimedia Commons)
Regulation of Renal Blood Flow
- Autoregulation
- The myogenic mechanism: where an increase in intravascular pressure stimulates stretch receptors in the vessel wall causing a reflex smooth muscle contraction and hence vessel vasoconstriction and reduced flow.
- The tubuloglomerular feedback mechanism: where an increase in tubular flow rate (with a resultant increase in tubular NaCl concentration detected by the macula densa) causes the juxtaglomerular apparatus to release adenosine which produces afferent arteriolar vasoconstriction and reduces GFR.
- Renin-Angiotensin II system
- The juxtaglomerular apparatus releases renin in response to a drop in afferent arteriolar pressure, a fall in tubular flow rate, or a fall in tubular NaCl concentration at the macula densa.
- Other stimuli to renin release include sympathetic nerve stimulation of beta1-adrenergic receptors on granular cells and a fall in angiotensin II levels.
- Renin promotes the production of angiotensin II which acts to vasoconstrict afferent and efferent arterioles (the dominant effect is on efferent arteriolar constriction so the GFR is increased).
- Prostaglandins
- Many peripheral vasoconstrictors stimulate the renal production of vasodilating prostaglandins such as PGE2 and PGI2 (prostacyclin) which protect the kidney from severe vasoconstriction.
- Vasoactive peptides
- Bradykinin, released in the distal tubule and glomerulus, promotes prostaglandin synthesis and vasodilation.
- Natriuretic peptides, released from cardiac cells, produce systemic vasodilation.
- Endothelin, produced in renal vascular endothelial cells and tubules, is a potent vasoconstrictor.
- Vasopressin (ADH) promotes vasoconstriction and antidiuretic action.
- Adrenomedullin promotes renal vasodilation and is produced in the kidney.
- Other regulatory pathways
- Renal nerves contain sympathetic neurons which release noradrenaline which causes constriction of both afferent and efferent arterioles and promotes renin release.
- Dopamine at low doses has a vasodilatory effect. At higher concentrations dopamine causes renal vasoconstriction and promotes renin release.
- Nitric oxide is a potent vasodilator that is synthesised in the macula densa, endothelium and mesangial cells and upregulated in response to mechanical shear stress.
| Vasodilators | Vasoconstrictors |
|---|---|
| Prostaglandins | Angiotensin II |
| Nitric oxide | Endothelin |
| Bradykinin | Vasopressin |
| Low-dose dopamine | Noradrenaline |
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
