| Pharmacokinetics:
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After Oral
adminestiration, the peak plasma concentrations
are usually reached within 2-3 hours following
the oral administration. The absorption
of Ranitidine is not influenced by food
or antacids.
With an elimination half-life of approximately
2-3 hours, ranitidine is excreted via kidneys
in the free and metabolised forms. (N-oxide
is the main metabolite and S-oxide and desmethyl
ranitidine in smaller quantities.)
There is normally no interaction
between ranitidine and the cytochrome
P450-linked drug metabolising enzyme
system.
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| Effects on Other
Gastrointestinal Secretions: |
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Pepsin:
Ranitidine HCl does not affect pepsin
secretion. Total pepsin output is
reduced in proportion to the decrease
in volume of gastric juice.
Intrinsic
Factor: Ranitidine HCl has
no significant effect on pentagastrin-stimulated
intrinsic factor secretion.
Serum
Gastrin: Ranitidine HCl has
little or no effect on fasting or
postprandial serum gastrin. |
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| Other Pharmacologic
Actions : |
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a.
Gastric bacterial flora: Increase
in nitrate-reducing organisms, significance
not known.
b. Prolactin levels: No effect in
recommended oral or (IV) dosage, but
small, transient, dose-related increases
in serum prolactin have been reported
after IV bolus injections of 100 mg
or more.
c. Other pituitary hormones: No effect
on serum gonadotropins, TSH, or GH.
Possible impairment of vasopressin
release.
d. No change in cortisol aldosterone,
androgen, or estrogen levels.
e. No antiandrogenic action.
f. No effect on count, motility,
or morphology of sperm.
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