Target type: biologicalprocess
The process in which the volume of blood increases renal pressure and thereby results in both an increase in urine volume (diuresis) and an increase in the amount of sodium excreted in the urine (natriuresis). [GOC:mtg_cardio]
Pressure natriuresis is a physiological mechanism that regulates blood pressure by increasing sodium excretion in the urine in response to elevated blood pressure. This process involves a complex interplay of hormonal, neural, and renal mechanisms.
**Mechanism of Pressure Natriuresis:**
1. **Increased Arterial Pressure:** Elevated blood pressure triggers a cascade of events leading to sodium excretion.
2. **Renal Hemodynamic Changes:** Increased arterial pressure leads to increased renal blood flow and glomerular filtration rate (GFR). This results in a higher volume of fluid filtered through the glomerulus, increasing the delivery of sodium to the distal tubules.
3. **Hormonal and Neural Regulation:**
- **Atrial Natriuretic Peptide (ANP):** Stretch receptors in the atria detect increased blood volume and release ANP. ANP inhibits sodium reabsorption in the collecting duct, promoting sodium excretion.
- **Brain Natriuretic Peptide (BNP):** Similar to ANP, BNP is released from the ventricles in response to increased blood pressure and promotes natriuresis.
- **Renin-Angiotensin-Aldosterone System (RAAS):** Increased blood pressure suppresses the RAAS, reducing aldosterone secretion. Aldosterone normally promotes sodium reabsorption, so its suppression contributes to natriuresis.
- **Sympathetic Nervous System:** The sympathetic nervous system is also involved in the regulation of blood pressure. Increased blood pressure can trigger a decrease in sympathetic activity, which can reduce sodium reabsorption and contribute to natriuresis.
4. **Tubular Sodium Handling:** Increased sodium delivery to the distal tubules, coupled with hormonal and neural influences, promotes sodium excretion through various mechanisms:
- **Increased Sodium Excretion:** Sodium excretion is increased in the distal tubules and collecting ducts, primarily due to the actions of ANP and reduced aldosterone levels.
- **Reduced Sodium Reabsorption:** ANP and other factors inhibit the activity of sodium transporters, reducing sodium reabsorption in the proximal and distal tubules.
**Significance of Pressure Natriuresis:**
Pressure natriuresis is a crucial mechanism for maintaining blood pressure homeostasis. By effectively excreting sodium in response to elevated blood pressure, it prevents excessive fluid retention and reduces the risk of hypertension and its associated complications.
**Disruption of Pressure Natriuresis:**
Disruption of pressure natriuresis can contribute to the development of hypertension. Factors that impair pressure natriuresis include:
- **Renal disease:** Impaired renal function can reduce the ability of the kidneys to excrete sodium.
- **Heart failure:** Heart failure can lead to increased blood pressure and reduced ANP production, impairing pressure natriuresis.
- **Hormonal imbalances:** Conditions that disrupt the RAAS or ANP production can also affect pressure natriuresis.
**In summary, pressure natriuresis is a complex physiological process that involves renal, hormonal, and neural mechanisms to maintain blood pressure homeostasis by increasing sodium excretion in response to elevated blood pressure.**'
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Protein | Definition | Taxonomy |
---|---|---|
Cytochrome P450 4A11 | A cytochrome P450 4A11 that is encoded in the genome of human. [PRO:DNx, UniProtKB:Q02928] | Homo sapiens (human) |
Cytochrome P450 4F2 | A cytochrome P450 4F2 that is encoded in the genome of human. [PRO:DNx, UniProtKB:P78329] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
17-octadecynoic acid | octadec-17-ynoic acid : An acetylenic fatty acid that is octadecanoi acid (stearic acid) which has been doubly dehydrogenated at positions 17 and 18 to give the corresponding alkynoic acid. | acetylenic fatty acid; long-chain fatty acid; monounsaturated fatty acid; terminal acetylenic compound | EC 1.14.14.94 (leukotriene-B4 20-monooxygenase) inhibitor; EC 1.14.15.3 (alkane 1-monooxygenase) inhibitor; P450 inhibitor |
ketoconazole | 1-acetyl-4-(4-{[2-(2,4-dichlorophenyl)-2-(1H-imidazol-1-ylmethyl)-1,3-dioxolan-4-yl]methoxy}phenyl)piperazine : A dioxolane that is 1,3-dioxolane which is substituted at positions 2, 2, and 4 by imidazol-1-ylmethyl, 2,4-dichlorophenyl, and [para-(4-acetylpiperazin-1-yl)phenoxy]methyl groups, respectively. | dichlorobenzene; dioxolane; ether; imidazoles; N-acylpiperazine; N-arylpiperazine | |
tranylcypromine | (1R,2S)-tranylcypromine : A 2-phenylcyclopropan-1-amine that is the (1R,2S)-enantiomer of tranylcypromine. tranylcypromine : A racemate comprising equal amounts of (1R,2S)- and (1S,2R)-2-phenylcyclopropan-1-amine. An irreversible monoamine oxidase inhibitor that is used as an antidepressant (INN tranylcypromine). Tranylcypromine: A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders. (From AMA Drug Evaluations Annual, 1994, p311) | 2-phenylcyclopropan-1-amine | |
proadifen hydrochloride | |||
pirlindole | pirlindole: RN given refers to parent cpd; synonym pyrazidol refers to mono-HCl; structure in Negwer, 5th ed, #2812 | carbazoles | |
17-dihydroexemestane | |||
kaf156 | ganaplacide: antimalarial |